|
|
||||||||
AJP - Lung Cellular and Molecular Physiology, Vol 270, Issue 2 298-L304, Copyright © 1996 by American Physiological Society
ARTICLES |
J. Khoury and D. Langleben
Division of Cardiology, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada.
Platelet-activating factor (PAF) is released from activated leukocytes and endothelial cells in sepsis, lung injury, and the adult respiratory distress syndrome. With these disorders, pulmonary hypertension develops, partly due to muscularization of the microvasculature by proliferation of pericytes. PAF may be a mediator of this process. Therefore, we examined the effects of PAF on in vitro growth of rat lung pericytes. Compared with control growth, semisynthetic PAF (10(-9) M) stimulated the 7-day mean growth of proliferating pericytes by 31% in medium with serum and 29% without serum and of previously growth-arrested pericytes by 12% with serum and 23% without serum. These effects were blocked by the PAF-receptor blocker CV-3988. PAF also increased [3H]thymidine incorporation into pericytes by 79%. Synthetic 16:0 PAF stimulated pericyte growth, but 18:0 PAF did not. PAF exposure did not induce apoptosis in pericytes. Thus PAF compounds, similar to those found in vivo, stimulate lung pericyte growth in vitro. PAF may act as a direct cytokine on cells involved in muscularization of the pulmonary vessel walls.
This article has been cited by other articles:
![]() |
J. Khoury and D. Langleben Heparin-like molecules inhibit pulmonary vascular pericyte proliferation in vitro Am J Physiol Lung Cell Mol Physiol, August 1, 2000; 279(2): L252 - L261. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |