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Protein kinase C-delta is involved in the inflammatory effect of IL-6 in mouse adipose cells

E Wallerstedt1, U Smith, C X Andersson

  • 1The Lundberg Laboratory for Diabetes Research, Center of Excellence for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine/Diabetes, The Sahlgrenska Academy at University of Gothenburg, Blå Stråket 5, SE-413 45, Gothenburg, Sweden.

Diabetologia
|February 13, 2010
PubMed
Abstract

Insights

Protein kinase C-delta (PKCdelta) is crucial for IL-6-induced inflammation in fat cells by phosphorylating STAT3. Inhibiting PKCdelta reduces inflammatory gene activation, suggesting it as a therapeutic target.

Area of Science:

  • Cellular biology
  • Molecular signaling
  • Inflammation research

Background:

  • Interleukin-6 (IL-6) is a key cytokine in inflammatory processes.
  • Signal transducer and activator of transcription 3 (STAT3) is a critical mediator of IL-6 signaling.
  • Protein kinase C-delta (PKCdelta) involvement in cellular responses is increasingly recognized.

Purpose of the Study:

  • To investigate the role of PKCdelta in IL-6-induced STAT3 phosphorylation.
  • To determine PKCdelta's effect on inflammatory gene activation in adipose cells.
  • To explore PKCdelta as a potential therapeutic target for IL-6-mediated inflammation.

Main Methods:

  • Utilized differentiated 3T3-L1 adipocytes and PKCdelta-deficient mouse embryonic fibroblasts (MEFs).
  • Treated cells with IL-6 and/or insulin, with or without the PKCdelta inhibitor rottlerin.
  • Analyzed gene expression via real-time PCR and protein phosphorylation/localization via immunoblotting.

Main Results:

  • PKCdelta inhibition or deficiency significantly reduced STAT3 phosphorylation at Ser-727 and Tyr-705.
  • Reduced STAT3 nuclear translocation and subsequent transcription of inflammatory genes (SAA3, Hp, Il6, Socs3).
  • PKCdelta nuclear translocation upon IL-6 stimulation was observed and inhibited by rottlerin.

Conclusions:

  • PKCdelta plays a pivotal role in mediating IL-6-induced inflammatory gene expression in adipose cells.
  • PKCdelta is essential for IL-6-induced STAT3 activation and nuclear translocation.
  • PKCdelta represents a promising molecular target for developing anti-inflammatory therapies.

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