SLC7A5促进TGF-β1诱导的小鼠胚胎成纤维细胞活化和增殖OA

Objective To investigate the effect of solute carrier family 7 member 5(SLC7A5)on the activation and proliferation of mouse embryonic fibroblasts induced by transforming growth factor β1(TGF-β1).Methods The NIH-3T3 mouse embryonic fibro-blast line was incubated with TGF-β1 for 24 h,and the target genes were screened using a PCR array.The fibroblasts were transfected with lentiviral vectors carrying either sh-SLC RNA(for gene silencing)or r-SLC RNA(for gene re-expression).The expression levels of SLC7A5,α-smooth muscle actin(α-SMA),vimentin(Vim),and type Ⅰ collagen(COL-Ⅰ)were detected using Western blotting and real-time PCR.The CCK-8 assay was used to determine the fibroblast proliferation rate in each group.The intracellular reduction-oxidation status was detected using a DCFH-DA probe and a reduced glutathione detection kit.Results The SLC7A5 protein and mRNA expres-sion levels in the TGF-β1 group were higher than those in the PBS group(P<0.05).Moreover,the α-SMA,Vim,and COL-Ⅰ expression levels were lower in the sh-SLC group than in the non-virus-transfected control group(P<0.05).Additionally,the proliferation rate of the sh-SLC-transfected fibroblasts and their intracellular glutathione content were decreased and their accumulation of reactive oxygen spe-cies was aggravated(P<0.05).By contrast,these effects were reversed in the r-SLC group.Conclusion SLC7A5 promotes the TGF-β1-induced activation and proliferation of mouse embryonic fibroblasts and may play a role in regulating intracellular oxidative stress.There-fore,SLC7A5 is a potential target for therapies aimed at inhibiting the activation and proliferation of fibroblasts in fibrotic diseases.