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Background  Sox 9 is a major marker of chondrocyte differentiation. When chondrocytes are cultured  in vitro  they progressively de-differentiate and this is associated with a decline in Sox 9 expression. The active form of vitamin D, 1, 25 (OH) 2 D 3  has been shown to be protective of cartilage in both humans and animals. In this study equine articular chondrocytes were grown in culture and the effects of 1, 25 (OH) 2 D 3  upon Sox 9 expression examined. The expression of the transient receptor potential vanilloid (TRPV) ion channels 5 and 6 in equine chondrocytes  in vitro , we have previously shown, is inversely correlated with de-differentiation. The expression of these channels in response to 1, 25 (OH) 2 D 3  administration was therefore also examined.    Results  The active form of vitamin D (1, 25 (OH) 2 D 3 ) when administered to cultured equine chondrocytes at two different concentrations significantly increased the expression of Sox 9 at both. In contrast 1, 25 (OH) 2 D 3  had no significant effect upon the expression of either TRPV 5 or 6 at either the protein or the mRNA level.    Conclusions  The increased expression of Sox 9, in equine articular chondrocytes  in vitro , in response to the active form of vitamin D suggests that this compound could be utilized to inhibit the progressive de-differentiation that is normally observed in these cells. It is also supportive of previous studies indicating that 1α, 25-dihydroxyvitamin D 3  can have a protective effect upon cartilage in animals  in vivo . The previously observed correlation between the degree of differentiation and the expression levels of TRPV 5/6 had suggested that these ion channels may have a direct involvement in, or be modulated by, the differentiation process  in vitro . The data in the present study do not support this.

han'gug dongmul jawon gwahag hoeji/han-guk dongmul jawon gwahak hoeji/journal of animal science and technology

Influence of 1α, 25-dihydroxyvitamin D3 [1, 25(OH)2D3] on the expression of Sox 9 and the transient receptor potential vanilloid 5/6 ion channels in equine articular chondrocytes