© 2000 American Heart Association, Inc.
Vascular Biology |
Altered Flow–Induced Arterial Remodeling in Vimentin-Deficient Mice
From the Department of Pharmacology and Toxicology and Cardiovascular Research Institute Maastricht (P.M.H.S., H.v.E., G.E.F., J.G.R.D.M.), Universiteit Maastricht, Maastricht, the Netherlands; Institut National de la Santé et de la Recherche Médicale (INSERM) U141 (D.H., C.M.B., B.I.L.), IFR Circulation Lariboisière, Université Paris VII, Paris, France; and Unité de Biologie du Developpement (E.C.-G., F.L.-V.), Institute Pasteur, Paris, France.
Correspondence to Dr J.G.R. De Mey, Department of Pharmacology and Toxicology, Universiteit Maastricht, PO Box 616, 6200 MD Maastricht, Netherlands. E-mail j.demey{at}farmaco.unimaas.nl
Abstract—The endothelial cytoskeleton plays a key role in arterial responses to acute changes in shear stress. We evaluated whether the intermediate filament protein vimentin is involved in the structural responses of arteries to chronic changes in blood flow (BF). In wild-type mice (V+/+) and in vimentin-deficient mice (V-/-), the left common carotid artery (LCA) was ligated near its bifurcation, and 4 weeks later, the structures of the occluded and of the contralateral arteries were evaluated and compared with the structures of arteries from sham-operated mice. Body weight and mean carotid artery BF did not differ between the strains, but LCA and right carotid artery (RCA) diameter (737±14 µm [LCA] and 723±14 µm [RCA] for V-/- versus 808±20 µm [LCA] and 796±20 µm [RCA] for V+/+) and medial cross-sectional area (CSAm) were significantly smaller in V-/- (21±1 and 22±2x103 µm2 for LCA and RCA, respectively) than in V+/+ (28±2 and 28±3x103 µm2 for LCA and RCA, respectively). In V+/+, LCA ligation eliminated BF in the occluded vessel (before ligation, 0.35±0.02 mL/min) and increased BF from 0.34±0.02 to 0.68±0.04 mL/min in the RCA. In V-/-, the BF change in the occluded LCA was comparable (from 0.38±0.05 mL/min to zero-flow rates), but the BF increase in the RCA was less pronounced (from 0.33±0.02 to 0.50±0.05 mL/min). In the occluded LCA of V+/+, arterial diameter was markedly reduced (-162 µm), and CSAm was significantly increased (5x103 µm2), whereas in the high-flow RCA of V+/+, carotid artery diameter and CSAm were not significantly modified. In the occluded LCA of V-/-, arterial diameter was reduced to a lesser extent (-77 µm) and CSAm was increased to a larger extent (10x103 µm2) than in V+/+. In contrast to V+/+, the high-flow RCA of V-/- displayed a significant increase in diameter (52 µm) and a significant increase in CSAm (5x103 µm2). These observations provide the first direct evidence for a role of the cytoskeleton in flow-induced arterial remodeling. Furthermore, they dissociate (1) between acute and chronic arterial responses to altered BF, (2) between alterations of lumen diameter and wall mass during arterial remodeling, and (3) between developmental and imposed flow-induced arterial remodeling.
Key Words: vimentin • arterial remodeling • blood flow • mice • carotid arteries
This article has been cited by other articles:
 |
|
 |
|
  E. N.T.P. Bakker, H. L. Matlung, P. Bonta, C. J. de Vries, N. van Rooijen, and E. VanBavel Blood flow-dependent arterial remodelling is facilitated by inflammation but directed by vascular tone Cardiovasc Res, May 1, 2008; 78(2): 341 - 348. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. A. Korshunov, S. M. Schwartz, and B. C. Berk Vascular Remodeling: Hemodynamic and Biochemical Mechanisms Underlying Glagov's Phenomenon Arterioscler. Thromb. Vasc. Biol., August 1, 2007; 27(8): 1722 - 1728. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. N.T.P. Bakker, A. Pistea, J. A.E. Spaan, T. Rolf, C. J. de Vries, N. van Rooijen, E. Candi, and E. VanBavel Flow-Dependent Remodeling of Small Arteries in Mice Deficient for Tissue-Type Transglutaminase: Possible Compensation by Macrophage-Derived Factor XIII Circ. Res., July 7, 2006; 99(1): 86 - 92. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Tzima Role of Small GTPases in Endothelial Cytoskeletal Dynamics and the Shear Stress Response Circ. Res., February 3, 2006; 98(2): 176 - 185. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. G. R. De Mey, P. M. Schiffers, R. H. P. Hilgers, and M. M. W. Sanders Toward functional genomics of flow-induced outward remodeling of resistance arteries Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1022 - H1027. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. H.P. Hilgers, P. M.H. Schiffers, W. M. Aartsen, G. E. Fazzi, J. F.M. Smits, and J. G.R. De Mey Tissue Angiotensin-Converting Enzyme in Imposed and Physiological Flow-Related Arterial Remodeling in Mice Arterioscler. Thromb. Vasc. Biol., May 1, 2004; 24(5): 892 - 897. [Abstract] [Full Text]
|
|
|
|
|
|
V. A. Korshunov and B. C. Berk Flow-Induced Vascular Remodeling in the Mouse: A Model for Carotid Intima-Media Thickening Arterioscler. Thromb. Vasc. Biol., December 1, 2003; 23(12): 2185 - 2191. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. H.P. Hilgers, S. Bergaya, P. M.H. Schiffers, P. Meneton, C. M. Boulanger, D. Henrion, B. I. Levy, and J. G.R. De Mey Uterine Artery Structural and Functional Changes During Pregnancy in Tissue Kallikrein-Deficient Mice Arterioscler. Thromb. Vasc. Biol., October 1, 2003; 23(10): 1826 - 1832. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Myers, K. J. Harmon, V. Lindner, and L. Liaw Alterations of Arterial Physiology in Osteopontin-Null Mice Arterioscler. Thromb. Vasc. Biol., June 1, 2003; 23(6): 1021 - 1028. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Ibrahim, J. K. Miyashiro, and B. C. Berk Shear Stress Is Differentially Regulated Among Inbred Rat Strains Circ. Res., May 16, 2003; 92(9): 1001 - 1009. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. F. Davies, J. Zilberberg, and B. P. Helmke Spatial Microstimuli in Endothelial Mechanosignaling Circ. Res., March 7, 2003; 92(4): 359 - 370. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Loufrani, B. I. Levy, and D. Henrion Defect in Microvascular Adaptation to Chronic Changes in Blood Flow in Mice Lacking the Gene Encoding for Dystrophin Circ. Res., December 13, 2002; 91(12): 1183 - 1189. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Loufrani, Z. Li, B. I. Levy, D. Paulin, and D. Henrion Excessive Microvascular Adaptation to Changes in Blood Flow in Mice Lacking Gene Encoding for Desmin Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1579 - 1584. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. J. Sullivan and J. B. Hoying Flow-Dependent Remodeling in the Carotid Artery of Fibroblast Growth Factor-2 Knockout Mice Arterioscler. Thromb. Vasc. Biol., July 1, 2002; 22(7): 1100 - 1105. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Tuttle, T. L. Hahn, B. M. Sanders, F. A. Witzmann, S. J. Miller, M. C. Dalsing, and J. L. Unthank Impaired collateral development in mature rats Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H146 - H155. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kawashima, T. Yamashita, M. Ozaki, Y. Ohashi, H. Azumi, N. Inoue, K.-i. Hirata, Y. Hayashi, H. Itoh, and M. Yokoyama Endothelial NO Synthase Overexpression Inhibits Lesion Formation in Mouse Model of Vascular Remodeling Arterioscler. Thromb. Vasc. Biol., February 1, 2001; 21(2): 201 - 207. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Ceiler and J. G. R. De Mey Chronic NG-Nitro-L-Arginine Methyl Ester Treatment Does Not Prevent Flow-Induced Remodeling in Mesenteric Feed Arteries and Arcading Arterioles Arterioscler. Thromb. Vasc. Biol., September 1, 2000; 20(9): 2057 - 2063. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F Langa, C Kress, E Colucci-Guyon, H Khun, S Vandormael-Pournin, M Huerre, and C Babinet Teratocarcinomas induced by embryonic stem (ES) cells lacking vimentin: an approach to study the role of vimentin in tumorigenesis J. Cell Sci., January 10, 2000; 113(19): 3463 - 3472. [Abstract] [PDF]
|
|
|
|
|
|
C. L. Buus, F. Pourageaud, G. E. Fazzi, G. Janssen, M. J. Mulvany, and J. G.R. De Mey Smooth Muscle Cell Changes During Flow-Related Remodeling of Rat Mesenteric Resistance Arteries Circ. Res., July 20, 2001; 89(2): 180 - 186. [Abstract] [Full Text] [PDF]
|
|