© 1996 American Heart Association, Inc.
Articles |
Phenotypic Heterogeneity of Rat Arterial Smooth Muscle Cell Clones
Implications for the Development of Experimental Intimal Thickening
From the Department of Pathology, University of Geneva, CMU, Geneva, Switzerland.
Correspondence to Professor G. Gabbiani, Department of Pathology, CMU, 1, rue Michel-Servet, 1211 Geneva 4, Switzerland.
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Abstract |
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Abstract It is well accepted that smooth muscle cells (SMCs) cultured from normal rat arterial media have different morphological and biological features compared with SMCs cultured from experimental intimal thickening (IT) 15 days after endothelial injury. It is not known, however, whether the phenotypic modulation producing IT cells occurs in any medial SMCs or only in a particular SMC subpopulation. To distinguish among these possibilities, the phenotypic features of SMC clones derived from normal adult media and the IT 15 days after endothelial lesion were analyzed according to morphological appearance, replicative activity in the presence and absence of fetal calf serum, and [3H]thymidine incorporation and motile activity; these features were compared with those of the respective SMC parental populations. Two categories of SMC clones predominated: spindle clones, with morphological features similar to those of the parental population from the normal media, and epithelioid clones, with morphological features similar to those of the IT parental population. Both categories were present among clones produced from normal media and IT; however, spindle was more common among normal media clones, and epithelioid, among IT clones. The behavior in vitro was distinct for each category of clones and did not depend on their origin. Our results are compatible with the possibility that the SMC population of IT in vivo derives mainly from SMCs belonging to the category exhibiting epithelioid features in vitro.
Key Words: atheromatosis • restenosis • actin isoforms • cell movement • cell replication
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Introduction |
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Experimental arterial IT after endothelial injury represents the most-used model for restenosis and SMC accumulation during atheromatous plaque formation.1 It is well established that IT depends on migration of SMCs from the media and on their replication1 ; more recently, SMC apoptosis has been suggested as playing a role in IT evolution.2 SMC migration and replication result from the combined action of several cytokines, growth factors, and extracellular matrix components.1 3 These factors may act on all medial SMCs, as is generally accepted, or, alternatively, on SMCs that are selectively prone to produce the IT population upon appropriate stimulation. Cultured SMCs from IT 15 days after endothelial injury exhibit distinct morphological and biological features compared with SMCs from normal media.4 This observation supports the hypothesis that SMCs in the two situations are biologically different but does not distinguish between the two possibilities mentioned above. It is more and more evident that SMCs are heterogeneous in several respects, including their capacity to react to the stimuli that play a role in IT formation.5 6 7 Thus, IT development may also depend on the phenotype of SMCs that are subject to migratory and replicative stimuli.
SMC heterogeneity has been mainly demonstrated by culturing populations with different phenotypes or expressing different proteins from the media of animals at various ages,8 9 10 11 from different portions of the arterial tree,12 13 or from different portions of the same artery.4 14 Thus, distinct SMC populations can be obtained from the luminal portion of the normal aortic media compared with the abluminal portion,15 from the IT induced by endothelial injury compared with the underlying media,4 or from IT at different times after endothelial injury.14 SMC clones produced from the normal aortic media of rats at different ages also display different cytoskeletal features.16
To analyze whether the normal arterial media contains SMCs capable of expressing in vitro features present in the whole population of IT cells, we characterized SMC clones from the normal aortic media and IT 15 days after endothelial injury in adult rats. We report here that such SMC clones can be classified into distinct categories on the basis of their phenotypic features irrespective of their origin; moreover, a proportion of SMC clones obtained from normal media has the same phenotypic features of the SMC whole population derived from experimental IT 15 days after endothelial injury. These findings are compatible with the possibility that the SMC whole population of IT in vivo derives essentially from a small number of distinct SMCs resident in the normal media.
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Methods |
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Cell Culture and SMC Cloning
A total of 40 adult (6- to 8-week-old) Wistar rats were used. SMCs were isolated by enzymatic digestion9 14 from the thoracic aortic media and from the 15-day-old IT produced by removing the endothelium of the thoracic aorta by means of an inflated embolectomy catheter.17 18 Cells were plated at a density of approximately 3x103 cells/cm2 in DMEM (GIBCO) supplemented with 10% FCS (Biological Industries). Whole SMC populations were grown up to the fifth passage in the same medium. For cloning, SMCs were obtained from normal aortic media and IT 15 days after endothelial injury.16 Four cloning experiments per situation were performed. Cloning was performed 48 hours after plating of the primary culture, when the whole SMC population is still available; this procedure allows us to obtain isolated cells more easily than at the time of plating. SMCs were cloned by limiting dilution (0.5 or 0.75 cell/well) into FCS-coated 96-well plates in DMEM containing 20% FCS. Cloned SMCs were expanded up to the third passage under the same conditions; they were then cultured as the whole SMC populations.16 The number and features of clones were calculated from three experiments per condition. In all experiments, SMCs were studied between the sixth and 15th passages.
Cell Proliferation and [3H]Thymidine
Incorporation
For evaluation of proliferation, SMCs were plated in DMEM in the
presence of 10% FCS at a concentration of 18x103
cells/cm2 and were counted after 7 days by using a
hemocytometer. Cells were also plated in DMEM supplemented with 2%
PDS14 or in a synthetic medium (Monomed, CSL Ltd) at a
density of 7x103 cells/cm2 and were counted 7
days after plating by using a
fluorescence-activated cell sorter (FACScan,
Beckton Dickinson). The results were calculated as the ratio of counted
to seeded cells.
For [3H]thymidine incorporation, SMCs were plated at a concentration of 7x103 cells/cm2 and synchronized for 4 days in DMEM supplemented with 10-9 mol/L selenium, 10-9 mol/L insulin (both, Collaborative Research), and 5 µg/mL transferrin (SIT; GIBCO).19 Fresh medium plus 10% FCS and 0.1 µCi/mL [3H]thymidine (specific activity, 5 Ci·mmol-1·L-1; Amersham) were added for 16 hours. [3H]thymidine incorporation was evaluated by trichloracetic acid precipitation and counting in a scintillation counter (Beckman Instruments). Results were expressed as the ratio of total [3H]thymidine incorporation in FCS to total [3H]thymidine incorporation in SIT.
Cell Migration
For evaluation of cell migration, SMCs were plated in DMEM in
the presence of 10% FCS at a concentration of 11x103
cells/cm2. Confluent cultures were scratched with
silicone rubber to obtain an 0.8-mm-wide in vitro
wound.20 After 24 hours, migrating cells invading the
empty space were counted by using a Zeiss Axiophot photomicroscope
(Carl Zeiss), a charge-coupled device camera (type FMC-4005,
AVT-Horn), and a Zeiss VIDAS (Carl Zeiss) interactive
image-analysis system. Six randomly preselected fields
(length, 2.5 mm) were analyzed per experiment. Results were
calculated as the total number of migrated cells per field.
Immunofluorescence Staining
SMCs were cultured in the presence of 10% FCS and fixed at
subconfluence or confluence; results were similar in both conditions.
Double immunofluorescence staining was performed
directly in the Petri dish or on cytocentrifuged SMCs. A
mouse monoclonal IgG2a specific for 
-SMA,21 and three
affinity-purified rabbit polyclonal IgGs specific for
desmin,18 SM myosin heavy chains,22 and human
von Willebrand factor and reacting with rat von
Willebrand factor (Sigma) were used.9 Cell counts
were made on cytocentrifuged cells16 by using
the Zeiss interactive image-analysis system.
Statistical Analysis
Results are given as mean±SEM. For statistical evaluation, the
results were analyzed by means of Student's t test.
Differences were considered statistically significant at values of
P<.05.
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Results |
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Clone Morphology
Cloning efficiency, ie, the percentage of clones growing in 96-well dishes, and the percentage of clones obtained after expansion to the fifth passage were higher in clones derived from IT (41% and 24%, respectively) than in clones derived from normal media (15% and 7%, respectively) (Table 1
).
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Clear differences were noted in the morphology of normal media and IT whole SMC populations.4 14 SMCs cultured from normal media were spindle shaped and displayed the classic "hills-and-valleys" pattern at confluence. SMCs cultured from IT appeared epithelioid and grew in a single layer. Both phenotypes persisted up to the 15th passage.
Clones derived from both populations were heterogeneous in
their morphology and could be divided into four categories: (1)
spindle-shaped, corresponding to the hills-and-valleys
appearance; (2) epithelioid, polygonal cells growing in a monolayer;
(3) thin-elongated, which consisted of densely packed elongated
cells forming typical whorls; and (4) senescent, characterized by large
vacuolated cells that could not reach confluence (Fig 1). The proportions of these categories were different
in clones derived from normal media and IT (Table 2).
Spindle-shaped clones were the main phenotype among those
derived from normal media, whereas epithelioid clones were the most
common among those derived from IT (40% and 63% of the total number
of clones, respectively). Thin-elongated and senescent morphologies
were more common in clones derived from normal media than in those
derived from IT. Between the fifth and 15th passages several clones,
independent of their morphology, underwent senescent changes and were
discarded. Thus, independent of their origin, SMC clones could be
classified on the basis of their morphology into four categories.
Nevertheless, the predominance of a category appears to depend on the
origin of the clones. To see whether biological features of the
different clones are also independent of their origin, we studied six
spindle-shaped, six epithelioid, and four thin-elongated clones
for cell proliferation in the presence and absence of FCS,
[3H]thymidine incorporation, migration, and cytoskeletal
features. Half the clones of each category were randomly taken from
those of normal media and half from those of IT. Cell proliferation and
[3H]thymidine incorporation were similar among clones
having a similar morphology irrespective of their origin. Moreover,
spindle-shaped clones displayed features similar to those of the
whole SMC population isolated from normal media, whereas epithelioid
clones displayed features similar to those of the whole SMC population
derived from IT. For this reason we concentrated our efforts on the
analysis of these two clonal SMC populations.
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Replicative Features
Because SMCs generally continue to proliferate after reaching
confluence, in our clones we examined both cell number 7 days after
plating in the presence of 10% FCS, when cells are
postconfluent,16 and DNA synthesis by means of
[3H]thymidine incorporation after FCS stimulation of
growth-arrested subconfluent cultures.
In the presence of 10% FCS, the number of cells counted 7 days after
plating was higher in spindle-shaped than in epithelioid clones
(6.4±0.5 and 4.1±0.2, respectively, P<.01). The
proliferation rates of spindle-shaped and epithelioid clones did
not differ from those of normal media and IT whole SMC populations,
respectively (Fig 2A). SMCs from epithelioid clones
stopped growing when confluent (about the fifth day after plating),
which has been noted for whole SMC populations isolated from
IT.4 14 Thin-elongated clones showed a very high cell
proliferation rate (14.7±1.2) when compared with the other categories
and whole SMC populations (P<.001 in all cases).
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The [3H]thymidine incorporation rate, which was measured
16 hours after FCS was added in synchronized SMC clones, was lower in
spindle-shaped (2.6±0.2) than epithelioid (4.4±0.2;
P<.001) clones (Fig 2B
). The results of spindle-shaped
and epithelioid clones were similar to those of normal media and IT
whole SMC populations, respectively (Fig 2B). Thin-elongated clones
(2.1±1.1) behaved similarly to spindle-shaped clones. Thus,
although epithelioid cells (from clones or whole SMC populations) stop
growing at confluence, they incorporate more
[3H]thymidine than spindle-shaped cells when they are
stimulated by FCS after synchronization. This shows a further
biological difference between spindle and epithelioid SMC clones.
Because SMCs isolated from IT and cultured as a whole SMC population
grow in the presence of PDS,4 14 we tested whether
epithelioid clones behave similarly (Fig 2C). Epithelioid clones showed
a doubling of their cell number (2.1±0.3) in the presence of 2% PDS 6
days after plating, whereas spindle-shaped clones remained
quiescent (0.7±0.1; P<.05). Thin-elongated clones
behaved as the spindle-shaped clones did. As expected, normal media
whole SMC populations did not replicate in the presence of PDS, whereas
IT whole SMC populations showed an increase in cell number, an increase
that was also observed for epithelioid clones (Fig 2C).
Migration Activity
Migration experiments showed that spindle-shaped clones
display a migration activity lower than that of epithelioid clones
(95±3 and 197±26, respectively; P<.05) (Fig 3). Whole SMC populations from normal media behaved as
spindle-shaped clones; whole SMC populations from IT showed results
similar to those of epithelioid clones (Fig 3). Thin-elongated
clones showed a migration activity intermediate between that of
spindle-shaped and epithelioid clones (142±15).
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Cytoskeletal Features
Cytoskeletal features of whole SMC populations cultured from
normal media and IT were in accordance with previous
reports.9 14 16 The percentage of -SMA–positive cells
derived from normal media was higher than the one derived from
IT.14 No whole SMC population cells expressed desmin and
very few of them (<5%) contained SM myosin.14 16
Irrespective of their morphology, all clones expressed a percentage of
cells positive to -SMA and SM myosin heavy chains much higher than
those of the corresponding whole SMC populations. Moreover, unlike the
whole SMC populations,9 14 16 some clones showed
desmin-positive cells up to the 15th passage. Thus, in all clones,
>80% of SMCs expressed -SMA and 20% to 90% of cells expressed SM
myosin heavy chains (Table 3). Three of six tested
spindle-shaped clones contained desmin; surprisingly, all
thin-elongated clones expressed desmin in 10% to 30% of the
cells. The tested epithelioid clones were negative for this protein.
All SMC populations, particularly the IT whole SMC populations and the
epithelioid clones, did not express von Willebrand factor,
indicating that they did not contain endothelial
cells.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Our results indicate that when classified on the basis of well-accepted criteria such as cell morphology, FCS-dependent and FCS-independent growth, [3H]thymidine incorporation, migratory activity, and cytoskeletal protein content, SMC clones from the aortic media and from IT 15 days after endothelial injury fall into four main phenotypic categories: spindle, epithelioid, thin-elongated, and senescent. To our knowledge, ours is the first report of SMC clones derived from the normal adult media that display all the features of the SMC whole population derived from IT 15 days after endothelial injury. It is noteworthy that SMCs belonging to a given phenotypic category express similar features irrespective of their origin; moreover, we have not seen modulation in vitro among the four phenotypic categories with the exception that the first three can evolve into the senescent one. Spindle and epithelioid clones are the most frequent: their biological features correspond to those of the whole SMC populations cultured from the normal aortic media and the IT 15 days after endothelial injury, respectively.4 14 Interestingly, the proportion of spindle SMC clones is predominant among those obtained from the normal media, whereas the proportion of epithelioid clones is predominant among those obtained from IT. These results indicate that the potential to develop clones with the spindle or epithelioid phenotype is different in the SMC populations of normal media and IT and that there is a correlation between the phenotypic features of the whole SMC populations derived from the aortic media or IT and the phenotypic features of the majority of the clones derived from the same locations.
Due to their similarities with whole SMC populations, we concentrated our efforts in the comparison of spindle and epithelioid clones. Their biological features are distinct, and, as far as we have observed, noninterchangeable; this is compatible with the possibility that they derive from distinct precursor SMCs. Epithelioid clones grow independent of FCS, similar to the whole SMC population from IT.4 However, epithelioid clones (like the whole SMC population from IT) stop growing at confluence, even in the presence of FCS; this probably contributes to their epithelioid appearance and is at variance with spindle clones and with the whole SMC population from the normal aortic media of adult rats. It is noteworthy that epithelioid clones (like the whole population of IT) have a high [3H]thymidine incorporation when growing at low cell density. However, our data do not clarify whether epithelioid SMCs have a shorter lag phase or whether a larger amount of cells enter in S phase compared with spindle-shaped SMCs. These observations show that each of these clonal or whole SMC populations possesses some properties that do not exactly correspond to the definition of normal growth in vitro; this may result from autocrine production of growth factor8 and may reflect their behavior in vivo when stimulated by serum components.
The migratory activities of spindle and epithelioid clones differ significantly, albeit quantitatively, and coincide with those of the corresponding whole populations. These findings are not surprising if one considers that SMCs producing IT after endothelial injury in vivo display an important motile activity.23
The cytoskeletal features of all clones, irrespective of their origin,
are in agreement with those from other reports.16 It is
noteworthy that in general clones show more differentiated properties
compared with the whole SMC populations from both normal
media16 and IT.14 Thus, >80% of SMCs from
every clone are positive for -SMA, and all clones contain a
significant proportion of SM myosin heavy chain–positive cells.
The expression of this protein is a reliable marker of terminal SMC
differentiation.24 Moreover, some clones had a proportion
of desmin-positive cells, particularly the spindle and
thin-elongated clones. Desmin disappears in early phases of culture
in whole SMC populations.21 Our observations in clonal
populations are in line with the well-known cytoskeletal
heterogeneity of vascular SMCs in vivo.25
Further studies are needed to understand the mechanisms of the higher
capacity of in vitro differentiation of clonal SMC populations compared
with their respective parental populations. In any event, our results
confirm their SMC nature.
Several laboratories, including ours, have attempted to characterize
SMC whole populations from the aortic media of rats at different
ages.6 9 10 11 Fetal SMCs exhibit FCS-independent
growth,11 contrary to newborn and adult
SMCs.6 9 An SMC population derived from 12-day-old
rats also exhibits an epithelioid phenotype and FCS-independent
growth.10 Finally, old (
18 months) rats produce
epithelioid cells, which, however, do not stop growing at
confluence.8 Our results show that the epithelioid
serum-independent phenotype can be produced in vitro by
cloning SMCs of the normal media early in primary culture. Since the
whole SMC population from IT 15 days after endothelial
injury has an epithelioid phenotype,4 14 it is
plausible that the precursors for this SMC population are present
in the media at all ages; it is conceivable that these precursor cells
are the major source of SMCs in IT. Further studies are needed to
pinpoint the factors influencing the emergence of a given category of
SMCs when placed in culture or when stimulated in vivo by
endothelial injury.
The cytoskeletal features of SMCs present in IT 15 days after endothelial injury are those of poorly differentiated SMCs but become similar to those of normal medial SMCs 60 days after endothelial injury.26 Correspondingly, the whole population of SMCs cultured from IT 15 days after endothelial injury has epithelioid features, whereas the whole population of SMCs cultured from IT 60 days after endothelial injury has spindle features.4 14 The SMC number per unit volume in IT 60 days after endothelial injury is smaller than that of SMCs in IT 15 days after endothelial injury.26 These findings are compatible with the existence of at least two populations of SMCs, both in normal media and IT 15 days after endothelial injury. To explain the change at 60 days after endothelial injury, one can hypothesize an important decrease of one of the two populations, eg, by means of apoptosis,2 rather than a phenotype modulation, as is now generally accepted.26 We are now working to verify this possibility.
Evidence for SMC heterogeneity in vivo and in vitro has been produced by means of different criteria and by using, in general, whole SMC populations.4 5 6 7 8 9 10 11 12 13 14 15 16 24 27 Our present results are in line with these reports and extend the notion of heterogeneity to clonal SMC populations derived from both normal media and IT. Benditt and Benditt28 have proposed that human atheromatous plaques are essentially monoclonal; the present observation that SMCs are heterogeneous10 12 27 is compatible with this hypothesis.
In conclusion, with the limitation that in vitro results do not necessarily reflect in vivo properties, our results suggest that SMCs react heterogeneously to stimulation by serum growth factors when placed in culture and are compatible with the possibility that the SMC population of IT in vivo derives mainly from a subpopulation of medial SMCs capable of producing in vitro the epithelioid phenotype. Further studies analyzing the biochemical and biological properties of clonal populations29 may furnish tools capable of distinguishing their respective precursors in vivo.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was partially supported by the Swiss National Science Foundation (grant 31-40372.94). We thank K. Grandchamp for help in statistical analysis, E. Denkinger and J.C. Rumbeli for photographic work, and M. Vitali for typing the manuscript.
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Footnotes |
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Dr Göran Hansson kindly acted as Guest Editor for this manuscript.
Received December 1, 1995; accepted January 26, 1996.
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References |
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 E. Schordan, S. Welsch, S. Rothhut, A. Lambert, M. Barthelmebs, J.-J. Helwig, and T. Massfelder Role of Parathyroid Hormone-Related Protein in the Regulation of Stretch-Induced Renal Vascular Smooth Muscle Cell Proliferation J. Am. Soc. Nephrol., December 1, 2004; 15(12): 3016 - 3025. [Abstract] [Full Text] [PDF]
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A. Agrotis, P. Kanellakis, G. Kostolias, G. Di Vitto, C. Wei, R. Hannan, G. Jennings, and A. Bobik Proliferation of Neointimal Smooth Muscle Cells after Arterial Injury: DEPENDENCE ON INTERACTIONS BETWEEN FIBROBLAST GROWTH FACTOR RECEPTOR-2 AND FIBROBLAST GROWTH FACTOR-9 J. Biol. Chem., October 1, 2004; 279(40): 42221 - 42229. [Abstract] [Full Text] [PDF]
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 B. Hinz, P. Pittet, J. Smith-Clerc, C. Chaponnier, and J.-J. Meister Myofibroblast Development Is Characterized by Specific Cell-Cell Adherens Junctions Mol. Biol. Cell, September 1, 2004; 15(9): 4310 - 4320. [Abstract] [Full Text] [PDF]
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D. K. Hogarth, N. Sandbo, S. Taurin, V. Kolenko, J. M. Miano, and N. O. Dulin Dual role of PKA in phenotypic modulation of vascular smooth muscle cells by extracellular ATP Am J Physiol Cell Physiol, August 1, 2004; 287(2): C449 - C456. [Abstract] [Full Text] [PDF]
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 C. A. Argmann, C. G. Sawyez, S. Li, Z. Nong, R. A. Hegele, J. G. Pickering, and M. W. Huff Human Smooth Muscle Cell Subpopulations Differentially Accumulate Cholesteryl Ester When Exposed to Native and Oxidized Lipoproteins Arterioscler. Thromb. Vasc. Biol., July 1, 2004; 24(7): 1290 - 1296. [Abstract] [Full Text] [PDF]
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 V. Andres Control of vascular cell proliferation and migration by cyclin-dependent kinase signalling: new perspectives and therapeutic potential Cardiovasc Res, July 1, 2004; 63(1): 11 - 21. [Abstract] [Full Text] [PDF]
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 F. Dandre and G. K. Owens Platelet-derived growth factor-BB and Ets-1 transcription factor negatively regulate transcription of multiple smooth muscle cell differentiation marker genes Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2042 - H2051. [Abstract] [Full Text] [PDF]
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A. Khanna Concerted effect of transforming growth factor-{beta}, cyclin inhibitor p21, and c-myc on smooth muscle cell proliferation Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H1133 - H1140. [Abstract] [Full Text] [PDF]
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Y. Gui and X.-L. Zheng Epidermal Growth Factor Induction of Phenotype-dependent Cell Cycle Arrest in Vascular Smooth Muscle Cells Is through the Mitogen-activated Protein Kinase Pathway J. Biol. Chem., December 26, 2003; 278(52): 53017 - 53025. [Abstract] [Full Text] [PDF]
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L. Stiebellehner, M. G. Frid, J. T. Reeves, R. B. Low, M. Gnanasekharan, and K. R. Stenmark Bovine distal pulmonary arterial media is composed of a uniform population of well-differentiated smooth muscle cells with low proliferative capabilities Am J Physiol Lung Cell Mol Physiol, October 1, 2003; 285(4): L819 - L828. [Abstract] [Full Text] [PDF]
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H. Hao, G. Gabbiani, and M.-L. Bochaton-Piallat Arterial Smooth Muscle Cell Heterogeneity: Implications for Atherosclerosis and Restenosis Development Arterioscler. Thromb. Vasc. Biol., September 1, 2003; 23(9): 1510 - 1520. [Abstract] [Full Text] [PDF]
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M. S. Kumar and G. K. Owens Combinatorial Control of Smooth Muscle-Specific Gene Expression Arterioscler. Thromb. Vasc. Biol., May 1, 2003; 23(5): 737 - 747. [Abstract] [Full Text] [PDF]
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C. Castro, A. Diez-Juan, M. J. Cortes, and V. Andres Distinct Regulation of Mitogen-activated Protein Kinases and p27Kip1 in Smooth Muscle Cells from Different Vascular Beds. A POTENTIAL ROLE IN ESTABLISHING REGIONAL PHENOTYPIC VARIANCE J. Biol. Chem., February 7, 2003; 278(7): 4482 - 4490. [Abstract] [Full Text] [PDF]
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G. Gennaro, C. Menard, E. Giasson, S.-E. Michaud, M. Palasis, S. Meloche, and A. Rivard Role of p44/p42 MAP Kinase in the Age-Dependent Increase in Vascular Smooth Muscle Cell Proliferation and Neointimal Formation Arterioscler. Thromb. Vasc. Biol., February 1, 2003; 23(2): 204 - 210. [Abstract] [Full Text] [PDF]
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 A. Zalewski, Y. Shi, and A. G. Johnson Diverse Origin of Intimal Cells: Smooth Muscle Cells, Myofibroblasts, Fibroblasts, and Beyond? Circ. Res., October 18, 2002; 91(8): 652 - 655. [Full Text] [PDF]
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 Y. Sakomura, H. Nagashima, Y. Aoka, K. Uto, A. Sakuta, S. Aomi, H. Kurosawa, T. Nishikawa, and H. Kasanuki Expression of Peroxisome Proliferator-Activated Receptor-{gamma} in Vascular Smooth Muscle Cells Is Upregulated in Cystic Medial Degeneration of Annuloaortic Ectasia in Marfan Syndrome Circulation, September 24, 2002; 106(12_suppl_1): I-259 - I-263. [Abstract] [Full Text] [PDF]
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H. Hao, P. Ropraz, V. Verin, E. Camenzind, A. Geinoz, M. S. Pepper, G. Gabbiani, and M.-L. Bochaton-Piallat Heterogeneity of Smooth Muscle Cell Populations Cultured From Pig Coronary Artery Arterioscler. Thromb. Vasc. Biol., July 1, 2002; 22(7): 1093 - 1099. [Abstract] [Full Text] [PDF]
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S. Sartore, A. Chiavegato, E. Faggin, R. Franch, M. Puato, S. Ausoni, and P. Pauletto Contribution of Adventitial Fibroblasts to Neointima Formation and Vascular Remodeling: From Innocent Bystander to Active Participant Circ. Res., December 7, 2001; 89(12): 1111 - 1121. [Abstract] [Full Text] [PDF]
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A. Niemann-Jonsson, M. P.S. Ares, Z.-Q. Yan, D.-X. Bu, G. N. Fredrikson, L. Branen, I. Porn-Ares, A. H. Nilsson, and J. Nilsson Increased Rate of Apoptosis in Intimal Arterial Smooth Muscle Cells Through Endogenous Activation of TNF Receptors Arterioscler. Thromb. Vasc. Biol., December 1, 2001; 21(12): 1909 - 1914. [Abstract] [Full Text] [PDF]
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 J.-L. Bascands, J.-P. Girolami, M. Troly, I. Escargueil-Blanc, D. Nazzal, R. Salvayre, and N. Blaes Angiotensin II Induces Phenotype-Dependent Apoptosis in Vascular Smooth Muscle Cells Hypertension, December 1, 2001; 38(6): 1294 - 1299. [Abstract] [Full Text] [PDF]
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 J. E. Faber, N. Yang, and X. Xin Expression of alpha -Adrenoceptor Subtypes by Smooth Muscle Cells and Adventitial Fibroblasts in Rat Aorta and in Cell Culture J. Pharmacol. Exp. Ther., August 1, 2001; 298(2): 441 - 452. [Abstract] [Full Text] [PDF]
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 B. C. Berk Vascular Smooth Muscle Growth: Autocrine Growth Mechanisms Physiol Rev, July 1, 2001; 81(3): 999 - 1030. [Abstract] [Full Text] [PDF]
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A. Orlandi, A. Francesconi, D. Cocchia, A. Corsini, and L. G. Spagnoli Phenotypic Heterogeneity Influences Apoptotic Susceptibility to Retinoic Acid and cis-Platinum of Rat Arterial Smooth Muscle Cells In Vitro : Implications for the Evolution of Experimental Intimal Thickening Arterioscler. Thromb. Vasc. Biol., July 1, 2001; 21(7): 1118 - 1123. [Abstract] [Full Text] [PDF]
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M.-L. Bochaton-Piallat, A. W. Clowes, M. M. Clowes, J. W. Fischer, M. Redard, F. Gabbiani, and G. Gabbiani Cultured Arterial Smooth Muscle Cells Maintain Distinct Phenotypes When Implanted Into Carotid Artery Arterioscler. Thromb. Vasc. Biol., June 1, 2001; 21(6): 949 - 954. [Abstract] [Full Text] [PDF]
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S. Ribault, P. Neuville, A. Mechine-Neuville, F. Auge, A. Parlakian, G. Gabbiani, D. Paulin, and V. Calenda Chimeric Smooth Muscle-Specific Enhancer/Promoters : Valuable Tools for Adenovirus-Mediated Cardiovascular Gene Therapy Circ. Res., March 16, 2001; 88(5): 468 - 475. [Abstract] [Full Text] [PDF]
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K. L. Davenpeck, C. Marcinkiewicz, D. Wang, R. Niculescu, Y. Shi, J. L. Martin, and A. Zalewski Regional Differences in Integrin Expression : Role of {{alpha}}5{beta}1 in Regulating Smooth Muscle Cell Functions Circ. Res., February 16, 2001; 88(3): 352 - 358. [Abstract] [Full Text] [PDF]
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 K. Wallner, B. G. Sharifi, P. K. Shah, S. Noguchi, H. DeLeon, and J. N. Wilcox Adventitial remodeling after angioplasty is associated with expression of tenascin mRNA by adventitial myofibroblasts J. Am. Coll. Cardiol., February 1, 2001; 37(2): 655 - 661. [Abstract] [Full Text] [PDF]
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 A. J. Halayko and J. Solway Plasticity in Skeletal, Cardiac, and Smooth Muscle: Invited Review: Molecular mechanisms of phenotypic plasticity in smooth muscle cells J Appl Physiol, January 1, 2001; 90(1): 358 - 368. [Abstract] [Full Text] [PDF]
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M. W. Majesky Novel Genes for Mitogen-Independent Smooth Muscle Replication Circ. Res., September 29, 2000; 87(7): 532 - 534. [Full Text] [PDF]
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M. C. M. Weiser-Evans, P. E. Schwartz, N. A. Grieshaber, B. E. Quinn, S. S. Grieshaber, J. K. Belknap, P. M. Mourani, R. A. Majack, and K. R. Stenmark Novel Embryonic Genes Are Preferentially Expressed by Autonomously Replicating Rat Embryonic and Neointimal Smooth Muscle Cells Circ. Res., September 29, 2000; 87(7): 608 - 615. [Abstract] [Full Text] [PDF]
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P. Neuville, M.-L. Bochaton-Piallat, and G. Gabbiani Retinoids and Arterial Smooth Muscle Cells Arterioscler. Thromb. Vasc. Biol., August 1, 2000; 20(8): 1882 - 1888. [Full Text] [PDF]
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W.-G. Li, F. J. Miller Jr, M. R. Brown, P. Chatterjee, G. R. Aylsworth, J. Shao, A. A. Spector, L. W. Oberley, and N. L. Weintraub Enhanced H2O2-Induced Cytotoxicity in "Epithelioid" Smooth Muscle Cells : Implications for Neointimal Regression Arterioscler. Thromb. Vasc. Biol., June 1, 2000; 20(6): 1473 - 1479. [Abstract] [Full Text] [PDF]
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S.-W. Chan, L. Hegyi, S. Scott, N. R. B. Cary, P. L. Weissberg, and M. R. Bennett Sensitivity to Fas-Mediated Apoptosis Is Determined Below Receptor Level in Human Vascular Smooth Muscle Cells Circ. Res., May 26, 2000; 86(10): 1038 - 1046. [Abstract] [Full Text] [PDF]
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K. Matsumoto, K.-i. Hirano, S. Nozaki, A. Takamoto, M. Nishida, Y. Nakagawa-Toyama, M. Y. Janabi, T. Ohya, S. Yamashita, and Y. Matsuzawa Expression of Macrophage (M{phi}) Scavenger Receptor, CD36, in Cultured Human Aortic Smooth Muscle Cells in Association With Expression of Peroxisome Proliferator Activated Receptor-{gamma}, Which Regulates Gain of M{phi}-Like Phenotype In Vitro, and Its Implication in Atherogenesis Arterioscler. Thromb. Vasc. Biol., April 1, 2000; 20(4): 1027 - 1032. [Abstract] [Full Text] [PDF]
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A. Orlandi, M. Marcellini, and L. G. Spagnoli Aging Influences Development and Progression of Early Aortic Atherosclerotic Lesions in Cholesterol-Fed Rabbits Arterioscler. Thromb. Vasc. Biol., April 1, 2000; 20(4): 1123 - 1136. [Abstract] [Full Text] [PDF]
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E. Tchekneva, M. L. Lawrence, and B. Meyrick Cell-specific differences in ET-1 system in adjacent layers of main pulmonary artery. A new source of ET-1 Am J Physiol Lung Cell Mol Physiol, April 1, 2000; 278(4): L813 - L821. [Abstract] [Full Text] [PDF]
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L. Chen, G. Daum, J. W. Fischer, S. Hawkins, M.-L. Bochaton-Piallat, G. Gabbiani, and A. W. Clowes Loss of Expression of the {beta} Subunit of Soluble Guanylyl Cyclase Prevents Nitric Oxide-Mediated Inhibition of DNA Synthesis in Smooth Muscle Cells of Old Rats Circ. Res., March 17, 2000; 86(5): 520 - 525. [Abstract] [Full Text] [PDF]
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G. B. Chapman, W. Durante, J. D. Hellums, and A. I. Schafer Physiological cyclic stretch causes cell cycle arrest in cultured vascular smooth muscle cells Am J Physiol Heart Circ Physiol, March 1, 2000; 278(3): H748 - H754. [Abstract] [Full Text] [PDF]
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S. Patel, Y. Shi, R. Niculescu, E. H. Chung, J. L. Martin, and A. Zalewski Characteristics of Coronary Smooth Muscle Cells and Adventitial Fibroblasts Circulation, February 8, 2000; 101(5): 524 - 532. [Abstract] [Full Text] [PDF]
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N. J. McCarthy and M. Bennett The regulation of vascular smooth muscle cell apoptosis Cardiovasc Res, February 1, 2000; 45(3): 747 - 755. [Abstract] [Full Text] [PDF]
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D. M Templeton, Y. Zhao, and M. Y. Fan Heterogeneity in the response of vascular smooth muscle to heparin: altered signaling in heparin-resistant cells Cardiovasc Res, January 14, 2000; 45(2): 503 - 512. [Abstract] [Full Text] [PDF]
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Z.-q. Yan, A. Sirsjo, M.-L. Bochaton-Piallat, G. Gabbiani, and G. K. Hansson Augmented Expression of Inducible NO Synthase in Vascular Smooth Muscle Cells During Aging Is Associated With Enhanced NF-{kappa}B Activation Arterioscler. Thromb. Vasc. Biol., December 1, 1999; 19(12): 2854 - 2862. [Abstract] [Full Text] [PDF]
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M. G. Frid, A. A. Aldashev, R. A. Nemenoff, R. Higashito, J. Y. Westcott, and K. R. Stenmark Subendothelial Cells From Normal Bovine Arteries Exhibit Autonomous Growth and Constitutively Activated Intracellular Signaling Arterioscler. Thromb. Vasc. Biol., December 1, 1999; 19(12): 2884 - 2893. [Abstract] [Full Text] [PDF]
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L. D. Adams, J. M. Lemire, and S. M. Schwartz A Systematic Analysis of 40 Random Genes in Cultured Vascular Smooth Muscle Subtypes Reveals a Heterogeneity of Gene Expression and Identifies the Tight Junction Gene Zonula Occludens 2 as a Marker of Epithelioid "Pup" Smooth Muscle Cells and a Participant in Carotid Neointimal Formation Arterioscler. Thromb. Vasc. Biol., November 1, 1999; 19(11): 2600 - 2608. [Abstract] [Full Text] [PDF]
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H. K.F. Lau Regulation of proteolytic enzymes and inhibitors in two smooth muscle cell phenotypes Cardiovasc Res, September 1, 1999; 43(4): 1049 - 1059. [Abstract] [Full Text] [PDF]
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S. Li, S. Sims, Y. Jiao, L. H. Chow, and J. G. Pickering Evidence From a Novel Human Cell Clone That Adult Vascular Smooth Muscle Cells Can Convert Reversibly Between Noncontractile and Contractile Phenotypes Circ. Res., August 20, 1999; 85(4): 338 - 348. [Abstract] [Full Text] [PDF]
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 J. Raymond, A. C. Desfaits, D. Roy, and J. P. Muizelaar Fibrinogen and Vascular Smooth Muscle Cell Grafts Promote Healing of Experimental Aneurysms Treated by Embolization • Editorial Comment Stroke, August 1, 1999; 30(8): 1657 - 1664. [Abstract] [Full Text] [PDF]
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T. Christen, M.-L. Bochaton-Piallat, P. Neuville, S. Rensen, M. Redard, G. van Eys, and G. Gabbiani Cultured Porcine Coronary Artery Smooth Muscle Cells : A New Model With Advanced Differentiation Circ. Res., July 9, 1999; 85(1): 99 - 107. [Abstract] [Full Text] [PDF]
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K. Zibara, M.-C. Bourdillon, E. Chignier, C. Covacho, and J. L. McGregor Identification and Cloning of a New Gene (2A3-2), Homologous to Human Translational Elongation Factor, Upregulated in a Proliferating Rat Smooth Muscle Cell Line and in Carotid Hyperplasia Arterioscler. Thromb. Vasc. Biol., July 1, 1999; 19(7): 1650 - 1657. [Abstract] [Full Text] [PDF]
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P. Neuville, Z.-q Yan, A. Gidlof, M. S. Pepper, G. K. Hansson, G. Gabbiani, and A. Sirsjo Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RAR{alpha}-Dependent Signaling Pathway Arterioscler. Thromb. Vasc. Biol., June 1, 1999; 19(6): 1430 - 1436. [Abstract] [Full Text] [PDF]
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L. L. Demer and Y. Tintut Osteopontin : Between a Rock and a Hard Plaque Circ. Res., February 5, 1999; 84(2): 250 - 252. [Full Text] [PDF]
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A. J. Halayko, B. Camoretti-Mercado, S. M. Forsythe, J. E. Vieira, R. W. Mitchell, M. E. Wylam, M. B. Hershenson, and J. Solway Divergent differentiation paths in airway smooth muscle culture: induction of functionally contractile myocytes Am J Physiol Lung Cell Mol Physiol, January 1, 1999; 276(1): L197 - L206. [Abstract] [Full Text] [PDF]
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M.-L. Bochaton-Piallat, G. Gabbiani, and M. S. Pepper Plasminogen Activator Expression in Rat Arterial Smooth Muscle Cells Depends on Their Phenotype and Is Modulated by Cytokines Circ. Res., June 1, 1998; 82(10): 1086 - 1093. [Abstract] [Full Text] [PDF]
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C. M. Shanahan and P. L. Weissberg Smooth Muscle Cell Heterogeneity : Patterns of Gene Expression in Vascular Smooth Muscle Cells In Vitro and In Vivo Arterioscler. Thromb. Vasc. Biol., March 1, 1998; 18(3): 333 - 338. [Abstract] [Full Text] [PDF]
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Z.-q. Yan and G. K. Hansson Overexpression of Inducible Nitric Oxide Synthase by Neointimal Smooth Muscle Cells Circ. Res., January 23, 1998; 82(1): 21 - 29. [Abstract] [Full Text] [PDF]
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Z. Yang, B. S. Oemar, T. Carrel, B. Kipfer, F. Julmy, and T. F. Luscher Different Proliferative Properties of Smooth Muscle Cells of Human Arterial and Venous Bypass Vessels : Role of PDGF Receptors, Mitogen-Activated Protein Kinase, and Cyclin-Dependent Kinase Inhibitors Circulation, January 20, 1998; 97(2): 181 - 187. [Abstract] [Full Text] [PDF]
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M. G. Frid, A. A. Aldashev, E. C. Dempsey, and K. R. Stenmark Smooth Muscle Cells Isolated From Discrete Compartments of the Mature Vascular Media Exhibit Unique Phenotypes and Distinct Growth Capabilities Circ. Res., December 19, 1997; 81(6): 940 - 952. [Abstract] [Full Text]
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C. I. Seye, A.-P. Gadeau, D. Daret, F. Dupuch, P. Alzieu, L. Capron, and C. Desgranges Overexpression of the P2Y2 Purinoceptor in Intimal Lesions of the Rat Aorta Arterioscler. Thromb. Vasc. Biol., December 1, 1997; 17(12): 3602 - 3610. [Abstract] [Full Text]
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C. L. Seidel Cellular Heterogeneity of the Vascular Tunica Media : Implications for Vessel Wall Repair Arterioscler. Thromb. Vasc. Biol., October 1, 1997; 17(10): 1868 - 1871. [Full Text]
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L. Capron, J. Jarnet, D. Heudes, D. Joseph-Monrose, and P. Bruneval Repeated Balloon Injury of Rat Aorta : A Model of Neointima With Attenuated Inhibition by Heparin Arterioscler. Thromb. Vasc. Biol., September 1, 1997; 17(9): 1649 - 1656. [Abstract] [Full Text]
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M. G. Frid, E. C. Dempsey, A. G. Durmowicz, and K. R. Stenmark Smooth Muscle Cell Heterogeneity in Pulmonary and Systemic Vessels : Importance in Vascular Disease Arterioscler. Thromb. Vasc. Biol., July 1, 1997; 17(7): 1203 - 1209. [Abstract] [Full Text]
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S. Sartore, A. Chiavegato, R. Franch, E. Faggin, and P. Pauletto Myosin Gene Expression and Cell Phenotypes in Vascular Smooth Muscle During Development, in Experimental Models, and in Vascular Disease Arterioscler. Thromb. Vasc. Biol., July 1, 1997; 17(7): 1210 - 1215. [Abstract] [Full Text]
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T. Takahashi, Y. Kawahara, M. Okuda, H. Ueno, A. Takeshita, and M. Yokoyama Angiotensin II Stimulates Mitogen-activated Protein Kinases and Protein Synthesis by a Ras-independent Pathway in Vascular Smooth Muscle Cells J. Biol. Chem., June 20, 1997; 272(25): 16018 - 16022. [Abstract] [Full Text] [PDF]
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B. Su, S. Mitra, H. Gregg, S. Flavahan, M. A. Chotani, K. R. Clark, P. J. Goldschmidt-Clermont, and N. A. Flavahan Redox Regulation of Vascular Smooth Muscle Cell Differentiation Circ. Res., July 6, 2001; 89(1): 39 - 46. [Abstract] [Full Text] [PDF]
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S. Li, Y.-S. Fan, L. H. Chow, C. Van Den Diepstraten, E. van der Veer, S. M. Sims, and J. G. Pickering Innate Diversity of Adult Human Arterial Smooth Muscle Cells: Cloning of Distinct Subtypes From the Internal Thoracic Artery Circ. Res., September 14, 2001; 89(6): 517 - 525. [Abstract] [Full Text] [PDF]
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