Biomedical Science Letters (대한의생명과학회지)

The Korean Society for Biomedical Laboratory Sciences (대한의생명과학회)
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Paclitaxel Suppress Dedifferentiation via Mitogen-activated Protein Kinase Pathway in Rabbit Articular Chondrocyte

  • 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 (국립공주대학교 자연과학대학 생명과학과)
  • Published : 2009.03.31
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Abstract

Microtubule-interfering agents (MIAs), including paclitaxel, have been attributed in part to interference with microtubule assembly, impairment of mitosis, and changes in cytoskeleton. But the signaling mechanisms that link microtubule disarray to destructive or protective cellular responses are poorly understood. This study investigated the effect of paclitaxel on differentiation such as type II collagen expression and sulfated proteoglycan accumulation in rabbit articular chondrocytes. Paclitaxel caused differentiated chondrocyte phenotype as demonstrated by increment of type II collagen expression and proteoglycan synthesis Paclitaxel treatment stimulated activation of ERK-1/2 and p38 kinase. Inhibition of ERK-1/2 with PD98059 enhanced paclitaxel-induced differentiation, whereas inhibition of p38 kinase with SB203580 suppressed paclitaxel-induced differentiation. Our findings suggest that ERK-1/2 and p38 kinase oppositely regulate paclitaxel-induced differentiation in chondrocytes.

Keywords

References

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