Caveolin-1 regulates human trabecular meshwork cell adhesion, endocytosis, and autophagy
Publication in refereed journal


摘要Impaired trabecular meshwork (TM) outflow is implicated in the pathogenesis of primary open-angle glaucoma (POAG). We previously identified the association of a caveolin-1 (CAV1) variant with POAG by genome-wide association study. Here we report a study of CAV1 knockout (KO) effect on human TM cell properties. We generated human CAV1-KO TM cells by CRISPR/Cas9 technology, and we found that the CAV1-KO TM cells less adhered to the surface coating than the wildtype TM cells by 69.34% (P < 0.05), but showed no difference in apoptosis. Higher endocytosis ability of dextran and transferrin was also observed in the CAV1-KO TM cells (4.37 and 1.89-fold respectively, P < 0.001), compared to the wildtype TM cells. Moreover, the CAV1-KO TM cells had higher expression of extracellular matrix-degrading enzyme genes (ADMTS13 and MMP14) as well as autophagy-related genes (ATG7 and BECN1) and protein (LC3B-II) than the wildtype TM cells. In summary, results from this study showed that the CAV1-KO TM cells have reduced adhesion with higher extracellular matrix-degrading enzyme expression, but increased endocytosis and autophagy activities, indicating that CAV1 could be involved in the regulation of adhesion, endocytosis, and autophagy in human TM cells.
著者Wu ZG, Huang CK, Xu CY, Xie LJ, Liang JJ, Liu LF, Pang CP, Ng TK, Zhang MZ
期刊名稱Journal of Cellular Biochemistry
出版社Wiley: 12 months
頁次13382 - 13391
關鍵詞autophagy, caveolin-1, cell adhesion, endocytosis, trabecular meshwork
Web of Science 學科類別Biochemistry & Molecular Biology;Cell Biology;Biochemistry & Molecular Biology;Cell Biology

上次更新時間 2021-15-01 於 01:15