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Nitric oxide induces apoptosis via Ca2+-dependent processes in the pancreatic beta-cell line MIN6

M Nakata1, N Uto, I Maruyama

  • 1Department of Laboratory Medicine, Faculty of Medicine, Kagoshima University, Japan.

Cell Structure and Function
|March 4, 2000
PubMed

Insights

Excessive nitric oxide (NO) production triggers apoptosis in pancreatic beta-cells, a key factor in type 1 diabetes. This cell death involves increased calcium (Ca2+) and activated calpain protease.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Excessive nitric oxide (NO) production is implicated in the destruction of pancreatic beta-cells, a hallmark of type 1 diabetes.
  • NO-induced beta-cell death typically occurs via apoptosis.

Purpose of the Study:

  • To investigate the link between NO, calcium (Ca2+), protease activity, and apoptosis in beta-cells.
  • To elucidate the molecular mechanisms underlying NO-induced beta-cell apoptosis.

Main Methods:

  • Utilized three NO donors (SNAP, NOR3, NOC7) to induce apoptosis in MIN6 beta-cell line.
  • Measured cytosolic Ca2+ concentration ([Ca2+]i) and employed a Ca2+ chelator (BAPTA-AM) and calpain inhibitor.

Main Results:

  • NO donors induced apoptosis in MIN6 cells in a concentration-dependent manner.
  • SNAP treatment increased [Ca2+]i and triggered apoptosis.
  • SNAP-induced apoptosis was significantly inhibited by BAPTA-AM and a calpain inhibitor.

Conclusions:

  • Excessive NO production directly induces beta-cell apoptosis.
  • Increased intracellular Ca2+ concentration and subsequent calpain activation are critical mediators of NO-induced beta-cell death.

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