Heparin and pge2 inhibit dna synthesis in human airway smooth
muscle cells in culture.
Johnson, Peter Ra, Carol L Armour, Donna Carey, and Judith L Black.
Departments of Pharmacology and Pharmacy, The University of Sydney,
NSW, Australia 2006
APStracts 2:0094L, 1995.
An increase in the bulk of the airway smooth muscle is a
characteristic of asthma. Much of the research investigating the
mechanisms of this increase in muscle has focused on mediators which
are mitogenic for smooth muscle, while relatively few studies have
focused on mediators inhibiting mitogenesis. In this study we have
examined the effects of two mediators proposed as regulators of
smooth muscle proliferation, viz heparin and PGE2 on human airway
smooth muscle cells in culture stimulated with 1, 2.5, 5 and 10%
foetal bovine serum (FBS) and platelet derived growth factor AB
(PDGF), 50ng/ml. PGE2 had a biphasic effect on DNA synthesis in the
presence of 1%FBS, with 10-6M causing inhibition and 10-7M causing an
increase in DNA synthesis. PGE2 caused inhibition of DNA synthesis in
the presence of 2.5, 5 and 10%FBS. Heparin 10 and 100 U/ml caused an
inhibition of DNA synthesis induced by 1% FBS, while 100U/ml
inhibited DNA synthesis induced by 5 and 10% FBS . PGE2, 10-8, 10-7
and 10-6M inhibited the DNA synthesis induced by PDGF, while heparin
1, 10 and 100 U/ml had no effect. These results indicate that both
PGE2 and heparin may have a role in the control of human airway
smooth muscle cell growth.
Received 18 November 1994; accepted in final form 31 May 1995.
APS Manuscript Number L334-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.