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sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor

Yangbin Pan1, Jianxin Wan2, Yipeng Liu1

  • 1Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

Scientific Reports
|October 23, 2014
PubMed

Insights

Secretory phospholipase A2 (sPLA2 IB) binding to the M-type phospholipase A2 receptor (PLA2R) on podocytes induces kidney cell apoptosis. This interaction activates signaling pathways and increases arachidonic acid, contributing to glomerular disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • The M-type phospholipase A2 receptor (PLA2R) is present in human glomerular podocytes.
  • Group IB secretory phospholipase A2 (sPLA2 IB) is a PLA2R ligand with elevated levels in chronic renal failure.
  • The specific roles of PLA2R and sPLA2 IB in glomerular disease pathogenesis remain unclear.

Purpose of the Study:

  • To investigate the role of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases.
  • To elucidate the mechanism by which sPLA2 IB interacts with PLA2R and affects podocyte apoptosis.

Main Methods:

  • Analysis of PLA2R and serum sPLA2 IB levels in relation to podocyte apoptosis in kidney biopsies.
  • In vitro studies using human podocyte cell cultures to examine sPLA2 IB-PLA2R interactions.
  • Assessment of podocyte apoptosis, PLA2R expression, ERK1/2 and cPLA2α phosphorylation, and arachidonic acid (AA) content following sPLA2 IB treatment.
  • Utilizing PLA2R-silenced podocytes to evaluate the receptor's role in apoptosis.

Main Results:

  • Higher PLA2R and serum sPLA2 IB levels correlated with increased podocyte apoptosis in patients.
  • In vitro, sPLA2 IB binding to PLA2R on human podocytes induced apoptosis in a time- and concentration-dependent manner.
  • sPLA2 IB upregulated PLA2R, increased ERK1/2 and cPLA2α phosphorylation, and enhanced podocyte apoptosis.
  • PLA2R silencing attenuated sPLA2 IB-induced apoptosis, and sPLA2 IB increased podocyte AA content.

Conclusions:

  • sPLA2 IB induces human podocyte apoptosis through binding to PLA2R.
  • The sPLA2 IB-PLA2R interaction activates ERK1/2 and cPLA2α signaling pathways.
  • Increased podocyte arachidonic acid content is a consequence of the sPLA2 IB-PLA2R interaction, contributing to podocyte apoptosis and potentially glomerular diseases.

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