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Regulation of calcium-permeable TRPV2 channel by insulin in pancreatic beta-cells

Etsuko Hisanaga1, Masahiro Nagasawa, Kohjiro Ueki

  • 1Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.

Diabetes
|November 6, 2008
PubMed
Abstract

Insights

Transient Receptor Potential Vanilloid 2 (TRPV2) channels in pancreatic beta-cells are regulated by insulin. TRPV2 plays a key role in insulin secretion and beta-cell growth.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Ion Channels

Background:

  • Pancreatic beta-cells synthesize and secrete insulin.
  • Calcium-permeable cation channel TRPV2 is expressed in beta-cells.
  • The regulation and function of TRPV2 in beta-cells remain largely uncharacterized.

Purpose of the Study:

  • To investigate the regulation of TRPV2 by insulin in pancreatic beta-cells.
  • To elucidate the role of TRPV2 in beta-cell function, including insulin secretion and growth.

Main Methods:

  • TRPV2 translocation was assessed in MIN6 cells and primary mouse beta-cells using fluorescent and c-Myc tagged TRPV2.
  • Calcium entry was measured using fura-2 fluorescence.
  • TRPV2 and insulin receptor (IR) knockdown were performed using shRNA.

Main Results:

  • Exogenous insulin induced TRPV2 translocation to the plasma membrane, increasing calcium entry, which was blocked by TRPV2 inhibition or knockdown.
  • High glucose also induced TRPV2 translocation, and its effect on insulin secretion and cell growth was inhibited by TRPV2 knockdown or tranilast.
  • Insulin-induced TRPV2 translocation was dependent on the insulin receptor.

Conclusions:

  • TRPV2 is regulated by insulin in pancreatic beta-cells.
  • TRPV2 is involved in the autocrine action of insulin, modulating insulin secretion and beta-cell growth.

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