TRPV4, a Ca ion channel plays pivotal role in chondrogenic mechanotransduction in ATDC5

众所周知，软骨细胞的代谢活动部分受物理因素的调节。然而，在软骨细胞中负责感知和转导的特定细胞机械传感器尚未完全确定。已有报道TRPV4激活可通过SOX9途径参与软骨形成过程。在这项研究中，我们证明了TRPV4作为一种机械受体在软骨细胞中响应机械应力，并确定了导致软骨形成的细胞内机制。我们的结论是，机械应力促进ATDC5细胞软骨形成，增加SOX9 mRNA的表达。化学和siRNA抑制TRPV4抑制ATDC5细胞机械应力的软骨形成作用。补充RR和转染TRPV4 siRNA可抑制机械应力引起的Ca内流。

It is well known that chondrocyte metabolic activity is partly regulated by physical factors.However, the specific cellular mechanosensor responsible for perception and transduction has not been fully identified in chondrocytes. It has already reported that TRPV4 activation can contribute to the process of chondrogenesis via SOX9 pathway.In this study we demonstrated that TRPV4 works as a mechanoreceptor in response to mechanical stress in chondrocytes, and to determine the intracellular mechanisms leading to the chondorogensis. Our conclusions are as follow, Mechanical stress promoted chondorogensis in ATDC5 cells with increasing mRNA expression of SOX9. Inhibition of TRPV4 by chmical and siRNA suppressed chondrogenesis effect of mechanical stress in ATDC5 cells. Ca influx by mechanical stress was suppressed by RR supplementation and TRPV4 siRNA transfection.