The role of TGFβ1 stimulating ROCK I signal pathway to reorganize actin in a rat experimental model of developmental dysplasia of the hip.

Importance of actin organization in control of chondrocyte phenotype is well established, but little is known about the role of transforming growth factor-β1 (TFGβ1) in regulating of ROCK I signal pathway. Here, we investigated the role of the TGFβ1, a well-studied member of the TGF-β superfamily, in chondrogenesis. Newborn Rats were randomly assigned to developmental dysplasia of the hip (DDH) group and control group. The isolated hips were performed with HE staining and immunohistochemistry. The chondrocytes was isolated and stained by immunofluorescence. The relative quantification of TGFβ1 on mRNA level was determined using real-time RT-PCR, and its secretion in culture supernatant in each well was detected by means of ELISA. The expression of ROCK I and ROCK II was detected by means of Western Blot. The relative amounts of actin in detergent-soluble and insoluble fractions were determined. Furthermore, TGFβ1 were employed to stimulate normal primary culture chondrocytes in vitro. We found TFGβ1 significantly changed in acetabulum chondrocytes after mechanical overloading. Over expression of TFGβ1 was observed by means of RT-PCR and ELISA assay. The expression of ROCK I was significantly increased in DDH acetabulum chondrocytes compared with normal cells. The detergent-soluble actin was confirmed reorganization in DDH chondrocytes. Furthermore, TFGβ1 can stimulate the ROCK I signaling to modulate actin location in vitro. In conclusion, our data suggested that TFGβ1 expression suppresses chondrogenesis through the control of ROCK signaling and actin organization.