Activation of p38 MAPK is involved in endothelin-1-stimulated COX-2 expression in cultured feline esophageal smooth muscle cells
- Authors
- Song, Hyun Ju; Min, Young Sil; Shin, Chang Yell; Jeong, Ji Hoon; Sohn, Uy Dong
- Issue Date
- Aug-2006
- Publisher
- KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
- Keywords
- COX; esophageal smooth muscle cells; ET-1; ETB receptor; p38 MAPK; PGE(2)
- Citation
- MOLECULES AND CELLS, v.22, no.1, pp 44 - 50
- Pages
- 7
- Journal Title
- MOLECULES AND CELLS
- Volume
- 22
- Number
- 1
- Start Page
- 44
- End Page
- 50
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/24293
- DOI
- 10.1002/aoc.1009
- ISSN
- 1016-8478
0219-1032
- Abstract
- We investigated the possible role of p38 MAPK and ETB receptors in ET-1 induction of cyclooxygenase-2 (COX-2) and prostaglandin E-2 (PGE(2)) in cultured feline esophageal smooth muscle cells (ESMC). Confluent layers of ESMC were stimulated with 10 nM ET-1 and expression of COX-1 and COX-2, involvement of receptors, and activation of p38 MAPK, were examined by Western blot analysis. Levels of PGE2 induced by ET-1 were measured by Elisa. Using ETA and ETB antagonists (BQ-123 and BQ-788, respectively), the contribution of the ET receptors to COVI and COX-2 expression induced by ET-1 was determined. Western blot analysis revealed that treatment of ESMC with ET-1 resulted in transient expression of COX-2 and activation of p38 MAPK. Activation of p38 MAPK was maximal after 1 h. S13202190, a p38 MAPK inhibitor, reduced expression of COX-2, but not COX-1. ET-1-induced release of PGE2 was also blocked by S13202190. COX-2 expression was upregulated only via the ETB receptor, and COX-1 expression was not affected by either antagonist. Taken together, our data suggest that ET-1 causes p38 MAPK-dependent expression of COX-2 by interacting with ETB receptors on ESMC.
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Collections - College of Pharmacy > School of Pharmacy > 1. Journal Articles
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