연골세포의 탈분화 및 세포고사 억제를 위한 기전연구
Regulation of Interleukin-1β-induced Dedifferentiation and Apoptosis via p38 Mitogen-activated Protein Kinase pathway in Articular Chondrocytes
- 고려대학교 보건과학연구소
- 보건과학논집
- 保健科學論集 Vol.31 No.2
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2005.1291 - 98 (8 pages)
- 7
Interleukin-1 (IL-1)β in articular chondrocytes regulates differentiation, apoptosis, and inflammatory responses. It is still controversial, however, whether IL-1β induces chondrocytes dedifferentiation and death. We investigated the role of the mitogen-activated protein kinase (MAPK) subtypes on IL-1β-induced dedifferentiation and apoptosis, as indicated by the inhibition of type II collagen expression and proteoglycan synthesis of rabbit articular chondrocytes. IL-1β treatment did not affect activation of ERK-1/2, but stimulation of p38 kinase. Inhibition of phospho ERK-1/2 with PD98059 enhanced IL-1β-induced dedifferentiation, and apoptosis up to 13.5%, whereas inhibition of phospho p38 kinase with SB203580 inhibited dedifferentiation, and apoptosis. Our results indicate that SB203580, p38 kinase inhibitor, inhibits IL-1β-induced dedifferentiation, and apoptosis.
Abstract<BR>Ⅰ. 서론<BR>Ⅱ. 실험방법<BR>Ⅲ. 실험결과<BR>Ⅳ. 토의 및 결론<BR>참고문헌<BR>
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