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Adiponectin stimulates phosphorylation of AMP-activated protein kinase alpha in renal glomeruli

Philippe G Cammisotto1, Moïse Bendayan

  • 1Department of Pathology and Cell Biology, University of Montreal, 2900, bd Edouard-Montpetit, Montreal, QC, Canada, H3T 1J4.

Journal of Molecular Histology
|October 23, 2008
PubMed

Insights

This study found functional adiponectin receptors (ADIPOR1) in all kidney glomerulus cells. These receptors activate AMP-activated protein kinase (AMPK), suggesting a role in controlling oxidative stress and cell survival.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Adiponectin receptor ADIPOR1 activates AMP-activated protein kinase (AMPK).
  • AMPK plays a role in controlling oxidative stress and apoptosis.
  • The presence and function of ADIPOR1 in renal glomeruli were previously unclear.

Purpose of the Study:

  • To investigate the presence and function of ADIPOR1 in renal glomerular cells.
  • To determine if ADIPOR1 activation impacts AMPK signaling in glomeruli.
  • To elucidate the potential role of ADIPOR1-AMPK pathway in glomerular physiology.

Main Methods:

  • In vitro incubation of isolated rat glomeruli with adiponectin.
  • Protein analysis using Western blot.
  • High-resolution immunogold electron microscopy on kidney sections.

Main Results:

  • ADIPOR1 and catalytic AMPK subunits (alpha1, alpha2) were detected in rat glomeruli.
  • Adiponectin or AICAR treatment activated AMPK phosphorylation in isolated glomeruli.
  • Electron microscopy localized ADIPOR1 and AMPK to the plasma membrane of endothelial, mesangial, podocyte, and Bowman's capsule epithelial cells.

Conclusions:

  • Glomerular cells express a functional ADIPOR1 receptor.
  • ADIPOR1 activation leads to AMPK activation within glomerular cells.
  • The ADIPOR1-AMPK pathway may be crucial for regulating oxidative stress and cell survival in the glomerulus.

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