- P-ISSN 1010-0695
- E-ISSN 2288-3339
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- P-ISSN1010-0695
- E-ISSN2288-3339
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Regulation of Interleukin-1b-induced Dedifferentiation and Apoptosis via p38 Mitogen-activated Protein Kinase pathway in Articular Chondrocytes
Journal of Korean Medicine / Journal of Korean Medicine, (P)1010-0695; (E)2288-3339
2006, v.27 no.1, pp.220-228
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(2006). Regulation of Interleukin-1b-induced Dedifferentiation and Apoptosis via p38 Mitogen-activated Protein Kinase pathway in Articular Chondrocytes. Journal of Korean Medicine, 27(1), 220-228.
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Abstract
Objective: Interleukin-1 (IL-1)b in articular chondrocytes regulates differentiation, apoptosis, and inflammatory responses. It is still controversial, So, we investigated IL-1b induces chondrocytes dedifferentiation and death. Also, we studied the role of the mitogen-activated protein kinase (MAPK) subtypes on IL-1b-induced dedifferentiation and apoptosis. Methods : To evaluation of dedifferentiation by chemokines of chondrocytes, we assessed such as proteoglycan, collagen, MMP-3 and MMP-13 by RT-PCR analysis. Also, to assess of apoptosis effect by chemokines, we measured annexin V/Propidium iodode (PI) and sub G1 cells in chondrocytes by flowcytometric analysis. Results : IL-1b treatment did not affect activation of ERK-1/2, but stimulation of p38 kinase. Inhibition of phospho ERK-1/2 with PD98059 enhanced IL-1b-induced dedifferentiation, and apoptosis up to 13.5%, whereas inhibition of phospho p38 kinase with SB203580 inhibited dedifferentiation, and apoptosis. Conclusions: Our results indicate that SB203580, p38 kinase inhibitor, inhibits IL-1b-induced dedifferentiation, and apoptosis by the inhibition of type II collagen expression and proteoglycan synthesis of rabbit articular chondrocytes.
- keywords
- Interleukin-1 (IL-1)b, chondrocytes, dedifferentiation, mitogen-activated protein kinase (MAPK), apoptosis., Interleukin-1 (IL-1)b, chondrocytes, dedifferentiation, mitogen-activated protein kinase (MAPK), apoptosis.
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