| First Author | Gao J | Year | 2022 |
| Journal | Exp Cell Res | Volume | 410 |
| Issue | 2 | Pages | 112965 |
| PubMed ID | 34896075 | Mgi Jnum | J:327742 |
| Mgi Id | MGI:6861642 | Doi | 10.1016/j.yexcr.2021.112965 |
| Citation | Gao J, et al. (2022) Cxcl10 deficiency attenuates renal interstitial fibrosis through regulating epithelial-to-mesenchymal transition. Exp Cell Res 410(2):112965 |
| abstractText | IFN-gamma-inducible protein 10 (IP-10, CXCL10) has been widely demonstrated to be involved in multiple kidney pathological processes. However, the role of CXCL10 in renal fibrosis remains unclear. In this study, Cxcl10-de fi cient (Cxcl10(-/-)) mice were used to generate the unilateral ureteral obstruction (UUO) model. The level of renal fibrosis and inflammatory cell infiltration was examined in vivo and the effects of CXCL10 on EMT process of HK-2 cells was investigated in vitro. We observed that the injury degree of renal tissue and the collagen deposition levels were lighter and the expression of alpha-SMA, collagen I and fi bronectin was significantly reduced in Cxcl10(-/-) mice, while the expression of E-cadherin was increased. However, interstitial F4/80-positive macrophages and CD4-positive T lymphocytes were unaffected by knockout of Cxcl10. Furthermore, IFN-gamma or CXCL10 stimulation could obviously promote the expression of alpha-SMA, collagen I, fi bronectin and reduce the expression of E-cadherin in HK-2 cells, which could be inhibited by transfection of Cxcl10-siRNA. Our findings suggested Cxcl10 knockout could reduce renal dysfunction and inhibit renal fibrosis through regulating EMT process of renal tubular epithelial cells in murine UUO model. These results may provide a novel insight into the mechanism and a potential therapy target of renal fibrosis. |
