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Int J Clin Exp Pathol 2013;6(10):2129-2136
/ISSN:1936-2625/IJCEP1306023
Original Article
MAPK/ERK signal pathway involved expression of
COX-2 and VEGF by IL-1β induced in human
endometriosis stromal cells in vitro
1 1 1 1 1 2
Fengying Huang , Jing Cao , Qiuhong Liu , Ying Zou , Hongyun Li , Tuanfang Yin
1Department of Obstetrics and Gynecology, 2Department of Otorhinolaryngology, TheSecond Xiangya Hospital,
Central South University, Changsha, Hunan, China, 410011
Received June 23, 2013; Accepted August 1, 2013; Epub September 15, 2013; Published October 1, 2013
Abstract: Objective: Now there are more and more evidences that Cyclooxygenase-2 (COX-2) plays an important role
in angiogenesis of endometriosis (EMs). Vascular endothelial growth factor (VEGF) has a potent angiogenic activity.
However, it is worth studying about the regulating mechanism of COX-2/COX-1 and VEGF in the development of hu-
man endometriosis in vitro. The current study was designed to investigate the effect of 4 cytokines on COX-2/COX-1
expression and the effect of IL-1β on VEGF release in human endometriosis stromal cells (ESC), and to explore the
related signaling pathways involved in vitro. Methods: Isolation, culture and identification of ESC. Cells were treated
with 4 cytokines, and the inhibitor mitogen-activated protein-Erk (MEK) and the inhibitor p38 mitogen-activated
protein kinase (MAPK) prior to adding cytokine IL-1β. COX-2 protein expression was measured by western blot and
VEGF secretion was determined by ELISA. Results: Among four kinds of cytokines, IL-1β treatment increased COX-2
protein expression and VEGF release in three ESC, and TNF-α had the same effect on COX-2 protein level as IL-1β
only in ectopic and eutopic ESC, and MCSF had only slight effect on ectopic ESC. In contrast, cytokines had no effect
on COX-1 expression. We also demonstrated that MAPK reduced the s
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