Neonatal pancreatic pericytes support β-cell proliferation

Mol Metab. 2017 Oct;6(10):1330-1338. doi: 10.1016/j.molmet.2017.07.010. Epub 2017 Jul 19.


Objective: The maintenance and expansion of β-cell mass rely on their proliferation, which reaches its peak in the neonatal stage. β-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 β-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 β-cell line and primary cultured mouse β-cells.

Results: Our findings indicate that neonatal pancreatic pericytes are required and sufficient for β-cell proliferation. We observed impaired proliferation of neonatal β-cells upon in vivo depletion of pancreatic pericytes. Furthermore, exposure to pericyte-conditioned medium stimulated proliferation in cultured β-cells.

Conclusions: This study introduces pancreatic pericytes as regulators of neonatal β-cell proliferation. In addition to advancing current understanding of the physiological β-cell replication process, these findings could facilitate the development of protocols aimed at expending these cells as a potential cure for diabetes.

Keywords: Beta-cells; Islets; Neonatal pancreas; Pericytes; Vasculature.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cell Differentiation
  • Cell Line
  • Cell Proliferation / physiology
  • Cells, Cultured
  • Insulin-Secreting Cells / physiology*
  • Integrin beta1 / metabolism
  • Mice
  • Mice, Transgenic
  • Pancreas / physiology
  • Pericytes / cytology*
  • Pericytes / physiology*
  • Signal Transduction


  • Integrin beta1