Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Arteriosclerosis, Thrombosis, and Vascular Biology. 1993;13:748-757

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by San Antonio, J. D.
Right arrow Articles by Pukac, L. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by San Antonio, J. D.
Right arrow Articles by Pukac, L. A.

Arteriosclerosis and Thrombosis, Vol 13, 748-757, Copyright © 1993 by American Heart Association

ARTICLES

Isolation of heparin-insensitive aortic smooth muscle cells. Growth and differentiation

JD San Antonio, MJ Karnovsky, ME Ottlinger, R Schillig and LA Pukac
Department of Pathology, Harvard Medical School, Boston, MA 02115.

Previous work has shown heparin and heparan sulfates to be potent inhibitors of vascular smooth muscle cell (VSMC) growth. This laboratory has previously isolated a VSMC line insensitive to the antiproliferative action of heparin by subjecting VSMCs that grew out from rat aortic medial explants to continuous passage in media containing heparin at 200 micrograms/mL. In the present study, we have isolated two additional heparin-resistant (HR) cell lines and have used the HR cells to investigate cellular mechanisms responsible for the potent antiproliferative activity of heparin. In contrast to normal heparin-sensitive VSMCs, the HR cells were smaller, displayed elongated processes, and possessed altered growth characteristics; however, both HR and normal cells bound and internalized comparable amounts of heparin. Immunohistochemical detection of smooth muscle cell-specific actin in growth-arrested cells showed staining of nearly all normal VSMCs and of a much smaller percentage of HR cells; heparin treatment caused a marked increase in the percentage of HR cells expressing smooth muscle cell alpha-actin, indicating that the antiproliferative and differentiation-promoting actions of heparin are independent. Proteins from control VSMCs and HR cells were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and heparin affinity chromatography. Several proteins were expressed preferentially by either HR cells or normal VSMCs, with the most significant difference being the secretion of a high-affinity, heparin-binding protein (M(r), 38,000) by control VSMCs but not by HR cells. We conclude that the aortic VSMC population may give rise to HR cells under selective conditions and that their unique characteristics, such as alterations in their ability to produce heparin-binding proteins, will prove useful in deciphering the cellular mechanisms involved in heparin's regulation of VSMC growth and differentiation.


This article has been cited by other articles:


Home page
 J CARDIOVASC PHARMACOL THERHome page
B. M. Sasseen, B. D. Gray, D. Gal, R. Lorinc, D. C. Carpenter, B. D. Klugherz, and R. L. Wilensky
Local Delivery of a Hydrophobic Heparin Reduces Neointimal Hyperplasia After Balloon Injury in Rat Carotid but not Pig Coronary Arteries
Journal of Cardiovascular Pharmacology and Therapeutics, December 1, 2001; 6(4): 377 - 383.
[Abstract] [PDF]

Home page
 Cardiovasc ResHome page
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]

Home page
 Am. J. Respir. Crit. Care Med.Home page
K. OKADA, M. L. BERNSTEIN, W. ZHANG, D. P. SCHUSTER, and M. D. BOTNEY
Angiotensin-converting Enzyme Inhibition Delays Pulmonary Vascular Neointimal Formation
Am. J. Respir. Crit. Care Med., September 1, 1998; 158(3): 939 - 950.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
J. R. Sindermann and K. L. March
Heparin Responsiveness In Vitro as a Prognostic Tool for Vascular Graft Stenosis : A Tale of Two Cell Types?
Circulation, June 30, 1998; 97(25): 2486 - 2490.
[Full Text] [PDF]

Home page
 CirculationHome page
J. S. Refson, M. Schachter, M. K. Patel, A. D. Hughes, E. Munro, P. Chan, J. H. N. Wolfe, and P. S. Sever
Vein Graft Stenosis and the Heparin Responsiveness of Human Vascular Smooth Muscle Cells
Circulation, June 30, 1998; 97(25): 2506 - 2510.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. J. Halayko, E. Rector, and N. L. Stephens
Airway smooth muscle cell proliferation: characterization of subpopulations by sensitivity to heparin inhibition
Am J Physiol Lung Cell Mol Physiol, January 1, 1998; 274(1): L17 - L25.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
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]


ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 1993 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.