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Pathological cardiac hypertrophy is an inevitable forerunner of heart failure. Regardless of the etiology of cardiac hypertrophy, cardiomyocyte mitochondrial alterations are always observed in this context. The translocases of mitochondrial outer membrane (Tom) complex governs the import of mitochondrial precursor proteins to maintain mitochondrial function under pathophysiological conditions; however, its role in the development of pathological cardiac hypertrophy remains unclear. Here, we showed that Tom70 was downregulated in pathological hypertrophic hearts from humans and experimental animals. The reduction in Tom70 expression produced distinct pathological cardiomyocyte hypertrophy both in vivo and in vitro. The defective mitochondrial import of Tom70-targeted optic atrophy-1 triggered intracellular oxidative stress, which led to a pathological cellular response. Importantly, increased Tom70 levels provided cardiomyocytes with full resistance to diverse pro-hypertrophic insults. Together, these results reveal that Tom70 acts as a molecular switch that orchestrates hypertrophic stresses and mitochondrial responses to determine pathological cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

A retraction note for the article “The role of TGFb1 stimulating ROCK I signal pathway to reorganize actin in a rat experimental model of developmental dysplasia of the hip" that was published in the journal “Molecular and Cellular Biochemistry" is presented.