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Hypoxic myocytes produce growth factor that stimulates COX-2 production.

Women's Health Weekly

| January 01, 2004 | COPYRIGHT 2004 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2004 JAN 1 - (NewsRx.com & NewsRx.net) -- Hypoxic myocytes produce growth factor that stimulates COX-2 production.

According to published research from the United States, "there is increasing evidence that cyclooxygenase (COX)-2 possess both angiogenic and cardioprotective properties. We examined the effects of hypoxic cardiac myocytes (H9c2 cells) on COX-2 expression in human umbilical vein endothelial cells (HUVECs) to determine the pathway involved in COX-2 regulation. The medium from hypoxic (

"HMCM induced a transient increase of COX-2 mRNA expression at 1 and 3 hours without affecting the COX-1 mRNA level. A similar effect also observed in HMCM from cultured primary cardiac myocytes (rat neonatal cardiac myocytes). The increased COX-2 mRNA was associated with a time-dependent increase in COX-2 protein expression," reported G.F. Wu and colleagues, Harvard University, School of Medicine.

"COX-2 was significantly induced by VEGF (4.86[+ or -]1.03-fold) and IL-1beta; (3.93[+ or -]0.89-fold) and slightly increased by TNF-alpha; but not by FGF2, IGF-1, or PDGFs. Analysis of proteins secreted in HMCM showed increased levels of VEGF but not IL-1beta; or TNF-alpha;. The HMCM-induced COX-2 expression was inhibited by the addition of an anti-VEGF neutralizing antibody. VEGF induced endothelial cell COX-2 expression by both increasing COX-2 transcription and prolonging the COX-2 mRNA half-life," scientists said.

"Furthermore, staurosporine, a nonselective PKC inhibitor, prevented the induction of VEGF by hypoxia. Both a selective PKC-alpha; and -beta; inhibitor and an inducible nitric oxide ...

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