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  • Title: Cytokine-induced apoptosis inhibitor-1 causes dedifferentiation of rabbit articular chondrocytes via the ERK-1/2 and p38 kinase pathways.
    Author: Yu SM, Yeo HJ, Choi SY, Kim SJ.
    Journal: Int J Biochem Cell Biol; 2016 Nov; 80():10-18. PubMed ID: 27644154.
    Abstract:
    Cytokine-induced apoptosis inhibitor-1 (CIAPIN-1, formally named anamorsin) is a well-known regulator of apoptosis in many different cell types. Recently, it has been reported that some anti-apoptotic proteins are involved with the regulation of cell differentiation. However, relatively little is known about the role of CIAPIN-1 on rabbit articular chondrocytes differentiation. In this study, we investigated the effects of CIAPIN-1 in chondrocytes, focusing on extracellular signal-regulated kinase (ERK)-1/2 and p38 kinase signaling. CIAPIN-1 caused dedifferentiation, as determined by the inhibition of type II collagen expression and sulfated-proteoglycan synthesis. CIAPIN-1 activated ERK-1/2 and inactivated p38 kinase, as determined by the phosphorylation level of each protein. CIAPIN-1-induced ERK phosphorylation was abolished by the MEK inhibitor, PD98059, which also prevented the CIAPIN-1-induced loss of type II collagen expression. Inhibition of p38 kinase with SB203580 enhanced the decrease in type II collagen expression. Our findings collectively suggest that ERK-1/2 and p38 kinase regulate CIAPIN-1-induced dedifferentiation in rabbit articular chondrocytes.
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