Study On The Effect Of TSG-6 On The Apoptosis Of Human Keloid By Regulating PI3K/Akt-Bcl-2 Pathway

Background: Researchers have reached the consensus that keloid formation is due to skin damage and stimulate,the excessive apoptosis or reduction of fibroblast is one of the features of cytology,which cause disease with dysfunction or beautiful barriers.At present,there are many related researches but the mechanism is still not clear and there is no definite cure.Tumor necrosis factor alpha stimulating genes-6(TSG-6)has been proved to have anti-inflammatory effects of gene,the preliminary related research also suggests that TSG-6 protein have the function of the anti-inflammatory and inhibit scar formation,but the mechanism of how TSG-6proteins involved in keloid formation is still not clear.PI3K/Akt cell signaling pathway plays a more important role in the development of tumor cells,For example,the activation of this pathway is due to the proliferation of cells caused by the initiation of anti-apoptotic pathways,but in keloid cells,there are few reports on the regulation of PI3K/ Akt-Bcl-2 signaling pathway in TSG-6.First of all,this article will explore the the biological behavior of keloid fibroblasts under the TSG-6 control,secondly the paper will continue to explore PI3K/Akt-Bcl-2 signaling pathways that how to affect apoptosis mechanism of keloid by TSG-6.Objective:To study whether tumor necrosis factor-inducibe gene 6(TSG-6)influence the human keloid fibroblasts(HKF)apoptosis,and the mechanism underlying may contribute to regulateand control phosphatidylinositol 3 kinase(PI3K)/protein kinase B(Akt)-B cell lymphoma-2(Bcl-2)signal pathway.Methods: HKF were cultured.The lentiviral expression vector(p LVX-puro-TSG-6)and sh RNA vector(p LVX-sh RNA1-TSG-6)and empty plassmid vector were builded and transfected into human keloid fibroblast cells stably,then flow cytometry and CCK-8were used to estimate the apoptotic and proliferation in each group.Expression levels of PI3K?Akt?murine double minute 2(MDM2)?P53?Bcl-2 m RNA and protein in each group were detected by RT-PCR and Western Blot respectively.Results and Conclusion: In the group of TSG-6 over-expression,proliferation of human keloid fibroblasts(HKF)cells were restrained.In addition,comparing with the control group,the value of apoptosis rose obviously(t=4.443,P= 0.011).However,in the interference group,proliferation of human keloid fibroblasts was increased and apoptosis was inhibited largely(t= 3.827,P=0.019).There were no significant difference among the p LVX-puro control group,the p LVX-sh RNA1 control group and the human keloid fibroblasts group.RT-PCR and Western blot assay shown that compared with the group of control,TSG-6 over-expressed inhuman keloid fibroblasts cells inhibited the expression of PI3 K ? Akt ? MDM2 ? P53 ? Bcl-2,but enhanced the expression of P53(P<0.05).The opposite results were found in the interference group(P<0.05).There were no significant difference among the p LVX-puro control group,the p LVX-sh RNA1 control group and the human keloid fibroblasts group.TSG-6 negatively regulates the PI3K/Akt-Bcl-2 pathways thus promotes human keloid fibroblasts apoptosis and inhibits keloid proliferation.