| First Author | Endo A | Year | 2023 |
| Journal | Dev Cell | Volume | 58 |
| Issue | 19 | Pages | 1819-1829.e5 |
| PubMed ID | 37716356 | Mgi Jnum | J:342511 |
| Mgi Id | MGI:7538778 | Doi | 10.1016/j.devcel.2023.08.002 |
| Citation | Endo A, et al. (2023) Phagocytosis by macrophages promotes pancreatic beta cell mass reduction after parturition in mice. Dev Cell 58(19):1819-1829.e5 |
| abstractText | Elucidating the mechanism(s) modulating appropriate tissue size is a critical biological issue. Pancreatic beta cells increase during pregnancy via cellular proliferation, but how beta cells promptly decrease to the original amount after parturition remains unclear. Herein, we demonstrate the role and mechanism of macrophage accumulation in this process. In the final stage of pregnancy, HTR1D signaling upregulates murine beta cell CXCL10, thereby promoting macrophage accumulation in pancreatic islets via the CXCL10-CXCR3 axis. Blocking this mechanism by administering an HTR1D antagonist or the CXCR3 antibody and depleting islet macrophages inhibited postpartum beta cell mass reduction. beta cells engulfed by macrophages increased in postpartum islets, but Annexin V administration suppressed this engulfment and the postpartum beta cell mass reduction, indicating the accumulated macrophages to phagocytose beta cells. This mechanism contributes to both maintenance of appropriate beta cell mass and glucose homeostasis promptly adapting to reduced systemic insulin demand after parturition. |
