Jia-Xuan Lei

The Second Xiangya Hospital of Central South University, Ch’ang-sha-shih, Hunan, China

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Publications (2)4.77 Total impact

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    ABSTRACT: This study aims to explore the function of Integrin-β/FAK in the mechanical signal transduction and the connection with downstream ERK signal pathways. Human osteosarcoma MG63 cell lines were used in this study. The effects of mechanical strain on the Integrin-β1 expression, FAK and ERK signal pathway in Human osteosarcoma MG63 cells were detected using RT-PCR and Western-blotting methods. The localization of FAK in Human osteosarcoma MG63 cells were determined using immunofluorescent method. The interaction between Integrin-β1 and FAK were detected by using co-immunoprecipitation method. The expression of Integrin-β1 shows a notable bimodel distribution, mechanical strain stimulation can promote Integrin-β1 expression and the phosphorylation of FAK and ERK, mechanical strain activated FAK and ERK mediated by Integrin-β1. Integrin-β1 may play an important role in osteoblast proliferation differentiation process, it might feel external strain stimulation through ECM composition and makes FAK phosphated through the interaction with FAK, thus causing a series of activation of signal molecules. Finally it reduces MAPK (ERK) activation and cellular responses to finish mechanical signal transduction.
    International journal of clinical and experimental pathology 12/2014; 7(11):7451-9. · 1.89 Impact Factor
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    ABSTRACT: To explore the possible role for connective tissue growth factor (CTGF) during tooth movement, we evaluated CTGF gene and protein expression in MG-63 cells subjected to cyclic stretch. Cyclic stretch caused a time-dependent increase in CTGF mRNA and protein levels.Inhibition of p38 MAP kinase or ERK activation did not affect cyclic stretch-induced CTGF expression. Specific inhibitors of PI3K suppressed stretch -induced CTGF expression in a time-dependent manner. cyclic stretch activated JNK and ERK, but not p38 MAP kinase in osteoblast-like cells. PI3K inhibitors suppressed cyclic stretch-induced JNK, but not p38 MAP kinase activation. Finally, SP600125, a Specific Inhibitor of JNK, suppressed stretch -induced CTGF Expression. These results suggest that stretch-induced CTGF expression is mediated through the PI3K-JNK -dependent pathway, not by p38 MAP kinase and ERK pathways.
    Cellular Physiology and Biochemistry 08/2011; 28(2):297-304. DOI:10.1159/000331743 · 2.88 Impact Factor