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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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PKCδ knockdown inhibits free fatty acid induction of endothelial cell apoptosis

Feiyan Yang1, Wei Cai, Kai Yang

  • 1Department of Cardiology, The Central Hospital of Wuhan, Wuhan, Hubei Province, China, 430014.

Cell Biochemistry and Function
|October 23, 2012
PubMed

Insights

Free fatty acids induce endothelial cell apoptosis, potentially through protein kinase C delta (PKCδ) and its interaction with the Fas pathway. Inhibiting PKCδ reduces this apoptosis, suggesting a key role for PKCδ in this cellular process.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Molecular Medicine

Background:

  • Endothelial cell apoptosis is a critical process in vascular health and disease.
  • The precise mechanisms by which free fatty acids trigger endothelial cell death remain incompletely understood.
  • Protein kinase C delta (PKCδ) and the Fas signaling pathway are implicated in apoptosis, but their specific roles in free fatty acid-induced endothelial cell apoptosis require elucidation.

Purpose of the Study:

  • To investigate the role of PKCδ in free fatty acid-induced endothelial cell apoptosis.
  • To explore potential apoptosis-related interactions between PKCδ and the Fas signal pathway in endothelial cells.

Main Methods:

  • Human umbilical vein endothelial cells were treated with varying concentrations of free fatty acids.
  • PKCδ and Fas expression were inhibited using small interfering RNA (siRNA).
  • Cell proliferation, apoptosis, and protein expression (p-PKCδTyr512, PKCδ, Fas) were quantified using colorimetric assays, flow cytometry, and Western blotting, respectively.

Main Results:

  • Free fatty acids inhibited cell proliferation and induced apoptosis in a concentration-dependent manner.
  • Treatment with free fatty acids increased Fas, PKCδ expression, and PKCδ phosphorylation.
  • Inhibition of PKCδ via siRNA attenuated free fatty acid-induced apoptosis and Fas expression.
  • Fas siRNA inhibited Fas expression but did not affect PKCδ expression or free fatty acid-induced apoptosis.

Conclusions:

  • PKCδ plays a significant role in mediating free fatty acid-induced endothelial cell apoptosis.
  • The pro-apoptotic effects of free fatty acids on endothelial cells may involve the upregulation of the PKCδ/Fas signaling axis.
  • Targeting PKCδ could represent a therapeutic strategy for conditions involving free fatty acid-induced endothelial dysfunction.
Keywords:
Fasdiabetesdysfunctionproliferationvascular

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