Paclitaxel Stimulates Cyclooxygenase-2 Expression via MAP Kinase Pathway in Rabbit Articular Chondrocytes

  • Im, Jeong-Hee (Department of Biological Sciences, College of Natural Sciences, Kongju National University) ;
  • Kim, Song-Ja (Department of Biological Sciences, College of Natural Sciences, Kongju National University)
  • ;
  • 김송자 (공주대학교 자연과학대학 생명과학과)
  • Published : 2009.06.30

Abstract

Paclitaxel, an antimicrotubule agent, binds to beta-tubulin in the microtubule and stabilizes the polymer, thereby repressing dynamic instability. Here, we have demonstrated that microtubule cytoskeletal architecture involved in regulation of the COX-2 expression in chondrocyte treated with paclitaxel. Paclitaxel enhanced COX-2 expression and prostaglandin E2 production, as indicated by the Western blot analysis, reverse transcriptase PCR(RT-PCR) and immunofluorescence staining, and $PGE_2$ assay, respectively. In our previous data have shown that paclitaxel treatment stimulated activation of ERK-1/2 and p38 kinase(Im et al., 2009). SB203580, an inhibitor of p38 kinase, blocked the induction of COX-2 expression by paclitaxel. Also PD98059, an inhibitor of ERK-1/2 kinase was blocked the induced COX-2 expression. These results indicate that activation of ERK-1/2 and p38 kinase is required for COX-2 expression induced by paclitaxel in rabbit articular chondrocytes.

Keywords

References

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