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KMID : 0613820110210040534
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Journal of Life Science
2011 Volume.21 No. 4 p.534 ~ p.541
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Retinoic Acid Potentiates Nitric Oxide-Induced Dedifferentiation through the ERK Pathway in Rabbit Articular Chondrocytes
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Yu Seon-Mi
Kim Song-Ja
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Abstract
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Retinoic acid (RA), a metabolite of vitamin A, is known to regulate dedifferentiation of rabbit articular chondrocytes. The regulatory mechanism of dedifferentiation by RA is not yet understood. Thus, the effect of RA on the regulation of nitric oxide (NO)-induced dedifferentiation was investigated in rabbit articular chondrocytes. RA caused loss of the differentiated chondrocyte phenotype as demonstrated by inhibition of type Ⅱ collagen expression and proteoglycan synthesis. RA also accelerated NO-induced dedifferentiation in rabbit articular chondrocytes as detected by expression of type Ⅱ collagen and Sox-9 using Western blot analysis and production of sulfated proteoglycan using Alcain blue staining. Further, RA potentiated NO-induced activation of ERK. Inhibition of ERK with PD98059 (PD) recovered the expression of type Ⅱ collagen and Sox-9 and production of sulfate proteoglycan in NO-induced dedifferentiated chondrocytes by RA treatment. Our findings suggest that RA accelerates NO-induced dedifferentiation of rabbit articular chondrocytes via the ERK pathway.
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KEYWORD
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Chondrocytes, retinoic acid(RA), nitric oxide(NO), dedifferentiation
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