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P-Rex1 Mediates Glucose-Stimulated Rac1 Activation and Insulin Secretion in Pancreatic β-Cells

Vijayalakshmi Thamilselvan1,2, Suhadinie Gamage1,2, Ali Harajli1,2

  • 1Biomedical Research Service, John D. Dingell VA Medical Center, Detroit, MI, USA.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|December 21, 2020
PubMed
Abstract

Insights

Phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 1 (P-Rex1) is crucial for glucose-stimulated Rac1 activation and insulin secretion in pancreatic beta cells. Its role in regulating these processes was investigated.

Area of Science:

  • Cellular and Molecular Biology
  • Endocrinology
  • Signal Transduction

Background:

  • Phosphoinositide 3-kinase (PI3-kinase) signaling regulates islet function.
  • The specific role of downstream pathways, like P-Rex1, in beta-cells is not well understood.

Purpose of the Study:

  • To investigate the role of P-Rex1 in glucose-stimulated Rac1 activation.
  • To determine the involvement of P-Rex1 in insulin secretion from beta-cells.

Main Methods:

  • Utilized INS-1 832/13 beta-cells for experiments.
  • Employed siRNA to suppress P-Rex1 and RhoG expression.
  • Quantified insulin secretion using ELISA.
  • Assessed Rac1 activation via pull-down assays.

Main Results:

  • P-Rex1 is expressed in beta-cells and islets.
  • Knockdown of P-Rex1 impaired glucose-induced Rac1 activation and insulin secretion.
  • RhoG did not significantly affect glucose-stimulated insulin secretion.
  • PI3-kinase inhibition potentiated insulin secretion without altering Rac1 activation.

Conclusions:

  • P-Rex1 plays a significant role in regulating glucose-induced Rac1 activation.
  • P-Rex1 is a novel regulator of insulin secretion in pancreatic beta-cells.
Keywords:
Rac1; P-Rex1; Insulin secretion; G proteins; Guanine nucleotide exchange factors; Pancreatic β-cell

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