| First Author | Epshtein A | Year | 2017 |
| Journal | Mol Metab | Volume | 6 |
| Issue | 10 | Pages | 1330-1338 |
| PubMed ID | 29031732 | Mgi Jnum | J:262468 |
| Mgi Id | MGI:6161941 | Doi | 10.1016/j.molmet.2017.07.010 |
| Citation | Epshtein A, et al. (2017) Neonatal pancreatic pericytes support beta-cell proliferation. Mol Metab 6(10):1330-1338 |
| abstractText | OBJECTIVE: The maintenance and expansion of beta-cell mass rely on their proliferation, which reaches its peak in the neonatal stage. beta-cell proliferation was found to rely on cells of the islet microenvironment. We hypothesized that pericytes, which are components of the islet vasculature, support neonatal beta-cell proliferation. METHODS: To test our hypothesis, we combined in vivo and in vitro approaches. Briefly, we used a Diphtheria toxin-based transgenic mouse system to specifically deplete neonatal pancreatic pericytes in vivo. We further cultured neonatal pericytes isolated from the neonatal pancreas and combined the use of a beta-cell line and primary cultured mouse beta-cells. RESULTS: Our findings indicate that neonatal pancreatic pericytes are required and sufficient for beta-cell proliferation. We observed impaired proliferation of neonatal beta-cells upon in vivo depletion of pancreatic pericytes. Furthermore, exposure to pericyte-conditioned medium stimulated proliferation in cultured beta-cells. CONCLUSIONS: This study introduces pancreatic pericytes as regulators of neonatal beta-cell proliferation. In addition to advancing current understanding of the physiological beta-cell replication process, these findings could facilitate the development of protocols aimed at expending these cells as a potential cure for diabetes. |
