| First Author | Wang Q | Year | 2023 |
| Journal | Exp Cell Res | Volume | 422 |
| Issue | 1 | Pages | 113406 |
| PubMed ID | 36332684 | Mgi Jnum | J:331722 |
| Mgi Id | MGI:7387908 | Doi | 10.1016/j.yexcr.2022.113406 |
| Citation | Wang Q, et al. (2022) Sox9 is required in regeneration of pancreatic beta cells following injury. Exp Cell Res 422(1):113406 |
| abstractText | The reduction of insulin secretion due to pancreatic beta cell injury caused by autoimmune reaction is the pathological basis of Type 1 diabetes mellitus (T1DM). Therefore, seeking new molecular targets for alleviating pancreatic beta cell injury will provide experimental basis for the prevention and treatment of T1DM. SRY-box 9 (Sox9) is not only an important molecule regulating the development of various organs, but also its high expression can aggravate the pathological process of various diseases. In addition, Sox9(+) cells are also pancreatic progenitor cells, participating in pancreatic repair reaction induced by injury. In our study, elevated blood glucose and lack of pancreatic beta cells almost returned to normal over time after streptozotocin (STZ)-induced pancreatic beta cell damage, implying that pancreatic beta cells were regenerated after STZ-induced injury. In particular, the expression of Sox9 was significantly elevated during pancreatic beta cell regeneration. On this basis, we conducted in vitro experiments to verify whether overexpression of Sox9 could inhibit the damage of pancreatic beta cells by inflammatory factors. Our results showed that overexpression of Sox9 alleviated the damage of pancreatic beta cells by inflammatory factors and improved the inhibitory effect of inflammatory factors on insulin secretion of pancreatic beta cells. Unsurprising, blood glucose levels, insulin content and pancreatic beta cell number failed to return to near-normal levels timely after pancreatic beta cells specific knockout Sox9 mice were treated with STZ, further confirming the importance of Sox9 in facilitating pancreatic beta cell repair or regeneration. Our study indicate that enhanced Sox9 activity might protect pancreatic beta cells from autoimmune induced damage and thus improve the pathological process of T1DM. |
