help button home button Am J Pathol R & D Systems
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
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 reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Coffey, A. K.
Right arrow Articles by Karnovsky, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Coffey, A. K.
Right arrow Articles by Karnovsky, M. J.

American Journal of Pathology, Vol 120, 248-255, Copyright © 1985 by American Society for Investigative Pathology

REGULAR ARTICLES

Heparin inhibits mesangial cell proliferation in habu-venom-induced glomerular injury

AK Coffey and MJ Karnovsky

The authors have investigated the ability of anticoagulant heparin and nonanticoagulant heparin to inhibit mesangial-cell proliferation after the administration of habu (Trimeresurus flavorivids) snake venom to rats. Rats given injected habu venom exhibited glomerular capillary cystic lesions 6 to 24 hours later, and marked mesangial proliferation was noted within the cyst after 3 days. At 7 days 87% of these lesions (nodules) contained primarily mesangial cells embedded in a dense matrix and fibrin. A decrease in the frequency of nodules and the persistence of cysts indicate effective antiproliferative treatment. When anticoagulant heparin treatment extended from 18 hours after venom administration until sacrifice at 7 days, the percentage of nodules was reduced to 40%. Nonanticoagulant heparins resulted in some, but inconsistent, inhibition of mesangial-cell proliferation. The mechanism of the antiproliferative action of heparin on mesangial cells is not known but may be similar to that for vascular smooth muscle growth regulation. The authors suggest that endogenous heparin in the glomerular basement membrane and mesangial matrix may exert an antiproliferative effect under normal conditions. Loss of this inhibition due to glomerular damage might be reversed by the addition of exogenous heparin.


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
I. M. D. Pecly, R. G. Goncalves, E. P. Rangel, C. M. Takiya, F. S. Taboada, C. A. Martinusso, M. S. G. Pavao, and M. Leite Jr
Effects of low molecular weight heparin in obstructed kidneys: decrease of collagen, fibronectin and TGF-{beta}, and increase of chondroitin/dermatan sulfate proteoglycans and macrophage infiltration
Nephrol. Dial. Transplant., May 1, 2006; 21(5): 1212 - 1222.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
H. R. Mason, R. A. Nowak, C. C. Morton, and J. J. Castellot Jr.
Heparin Inhibits the Motility and Proliferation of Human Myometrial and Leiomyoma Smooth Muscle Cells
Am. J. Pathol., June 1, 2003; 162(6): 1895 - 1904.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1985 by the American Society for Investigative Pathology.