| First Author | Wang Z | Year | 2020 |
| Journal | J Cell Physiol | Volume | 235 |
| Issue | 3 | Pages | 2149-2160 |
| PubMed ID | 31389030 | Mgi Jnum | J:299868 |
| Mgi Id | MGI:6490756 | Doi | 10.1002/jcp.29119 |
| Citation | Wang Z, et al. (2020) miR-222 inhibits cardiac fibrosis in diabetic mice heart via regulating Wnt/beta-catenin-mediated endothelium to mesenchymal transition. J Cell Physiol 235(3):2149-2160 |
| abstractText | miR-222 participates in many cardiovascular diseases, but its effect on cardiac remodeling induced by diabetes is unclear. This study evaluated the functional role of miR-222 in cardiac fibrosis in diabetic mice. Streptozotocin (STZ) was used to establish a type 1 diabetic mouse model. After 10 weeks of STZ injection, mice were intravenously injected with Ad-miR-222 to induce the overexpression of miR-222. miR-222 overexpression reduced cardiac fibrosis and improved cardiac function in diabetic mice. Mechanistically, miR-222 inhibited the endothelium to mesenchymal transition (EndMT) in diabetic mouse hearts. Mouse heart fibroblasts and endothelial cells were isolated and cultured with high glucose (HG). An miR-222 mimic did not affect HG-induced fibroblast activation and function but did suppress the HG-induced EndMT process. The antagonism of miR-222 by antagomir inhibited HG-induced EndMT. miR-222 regulated the promoter region of beta-catenin, thus negatively regulating the Wnt/beta-catenin pathway, which was confirmed by beta-catenin siRNA. Taken together, our results indicated that miR-222 inhibited cardiac fibrosis in diabetic mice via negatively regulating Wnt/beta-catenin-mediated EndMT. |
