Importance of actin organization in control of chondrocyte phenotype is wellestablished, 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 ofthe 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 andimmunohistochemistry. The chondrocytes was isolated and stained byimmunofluorescence. The relative quantification of TGFβ1 on mRNA level wasdetermined using real-time RT-PCR, and its secretion in culture supernatant in eachwell was detected by means of ELISA. The expression of ROCK I and ROCK II wasdetected by means of Western Blot. The relative amounts of actin indetergent-soluble and insoluble fractions were determined. Furthermore, TGFβ1 wereemployed to stimulate normal primary culture chondrocytes in vitro. We found TFGβ1significantly changed in acetabulum chondrocytes after mechanical overloading. Overexpression of TFGβ1 was observed by means of RT-PCR and ELISA assay. The expressionof ROCK I was significantly increased in DDH acetabulum chondrocytes compared withnormal cells. The detergent-soluble actin was confirmed reorganization in DDHchondrocytes. Furthermore, TFGβ1 can stimulate the ROCK I signaling to modulateactin location in vitro. In conclusion, our data suggested that TFGβ1 expressionsuppresses chondrogenesis through the control of ROCK signaling and actinorganization.