| First Author | You X | Year | 2024 |
| Journal | Biochim Biophys Acta Mol Cell Res | Volume | 1871 |
| Issue | 8 | Pages | 119845 |
| PubMed ID | 39265887 | Mgi Jnum | J:358804 |
| Mgi Id | MGI:7732986 | Doi | 10.1016/j.bbamcr.2024.119845 |
| Citation | You X, et al. (2024) SRSF2 is essential for maintaining pancreatic beta-cell identity and regulating glucose homeostasis in mice. Biochim Biophys Acta Mol Cell Res 1871(8):119845 |
| abstractText | Diabetes is characterized by decreased beta-cell mass and islet dysfunction. The splicing factor SRSF2 plays a crucial role in cell survival, yet its impact on pancreatic beta cell survival and glucose homeostasis remains unclear. We observed that the deletion of Srsf2 specifically in beta cells led to time-dependent deterioration in glucose tolerance, impaired insulin secretion, decreased islet mass, an increased number of alpha cells, and the onset of diabetes by the age of 10 months in mice. Single-cell RNA sequencing (scRNA-seq) analyses revealed that, despite an increase in populations of unfolded protein response (UPR)-activated and undifferentiated beta cells within the SRSF2_KO group, there was a notable decrease in the expression of UPR-related and endoplasmic reticulum (ER)-related genes, accompanied by a loss of beta-cell identity. This suggests that beta cells have transitioned from an adaptive phase to a maladaptive phase in islets of 10-month-old SRSF2_KO mice. Further results demonstrated that deletion of SRSF2 caused decreased proliferation in beta cells within 3-month-old islets and Min6 cells. These findings underscore the essential role of SRSF2 in controlling beta-cell proliferation and preserving beta-cell function in mice. |
