| First Author | Shi Z | Year | 2024 |
| Journal | Dev Cell | Volume | 59 |
| Issue | 10 | Pages | 1233-1251.e5 |
| PubMed ID | 38569546 | Mgi Jnum | J:352942 |
| Mgi Id | MGI:7643099 | Doi | 10.1016/j.devcel.2024.03.012 |
| Citation | Shi Z, et al. (2024) The Notch-PDGFRbeta axis suppresses brown adipocyte progenitor differentiation in early post-natal mice. Dev Cell 59(10):1233-1251.e5 |
| abstractText | De novo brown adipogenesis holds potential in combating the epidemics of obesity and diabetes. However, the identity of brown adipocyte progenitor cells (APCs) and their regulation have not been extensively explored. Here, through in vivo lineage tracing and mouse modeling, we observed that platelet-derived growth factor receptor beta (PDGFRbeta)+ pericytes give rise to developmental brown adipocytes but not to those in adult homeostasis. By contrast, T-box 18 (TBX18)+ pericytes contribute to brown adipogenesis throughout both developmental and adult stages, though in a depot-specific manner. Mechanistically, Notch inhibition in PDGFRbeta+ pericytes promotes brown adipogenesis by downregulating PDGFRbeta. Furthermore, inhibition of Notch signaling in PDGFRbeta+ pericytes mitigates high-fat, high-sucrose (HFHS)-induced glucose and metabolic impairment in mice during their development and juvenile phases. Collectively, these findings show that the Notch/PDGFRbeta axis negatively regulates developmental brown adipogenesis, and its repression promotes brown adipose tissue expansion and improves metabolic health. |
