학술논문

Involvement of COX-2 in VEGF-induced angiogenesis via P38 and JNK pathways in vascular endothelial cells
Document Type
Report
Source
Cardiovascular Research. Feb 1, 2006, Vol. 69 Issue 2, p512, 8 p.
Subject
Cardiology
Vascular endothelial growth factor
Protein kinases
Endothelium
Gene expression
Language
English
ISSN
0008-6363
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cardiores.2005.09.019 Byline: GuiFu Wu (a)(b), Jincai Luo (c), Jamal S. Rana (a), Roger Laham (a), Frank W. Sellke (d), Jian Li (a) Keywords: COX-2; VEGF; Angiogenesis; MAPK; p38; JNK; HUVEC Abstract: Cyclooxygenase-2 (COX-2) is induced by hypoxic stimuli and is also involved in the process of angiogenesis. We previously demonstrated that vascular endothelial growth factor (VEGF) is one of the principal factors produced by hypoxic myocytes and is responsible for the induction of COX-2 expression in endothelial cells. Yet the signaling pathways by which VEGF modulates COX-2 gene expression are still less well defined. We therefore examined the regulation of VEGF-induced COX-2 expression by the mitogen-activated protein kinase (MAPK) family in endothelial cells. Author Affiliation: (a) Division of Cardiology, Beth Israel Deaconess Medical Center/Harvard Medical School, 330 Brookline Ave., Boston, MA 02215, USA (b) Division of Cardiology/First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China (c) Laboratory of Vascular Biology, Institute of Molecular Medicine, Peking University, Beijing, China (d) Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center/Harvard Medical School, 330 Brookline Ave., Boston, MA 02215, USA Article History: Received 15 April 2005; Revised 22 September 2005; Accepted 25 September 2005 Article Note: (miscellaneous) Time for primary review 21 days