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Inhibition of GSK3 differentially modulates NF-{kappa}B, CREB, AP-1 and {beta}-catenin signaling in hepatocytes, but fails to promote TNF-{alpha}-induced apoptosis

Journal Article · · Experimental Cell Research
 [1]; ; ; ;  [2];  [3]; ;  [4];  [5];  [1];  [2]
  1. Institute of Molecular Medicine and Cell Research, University of Freiburg (Germany)
  2. Department of Pharmaceutical Biology and Biotechnology, University of Freiburg (Germany)
  3. DSM Nutritional Products 4303 Kaiseraugst (Switzerland)
  4. Gastroenterology, Department of Medicine, University Hospital Freiburg (Germany)
  5. Department of Pharmaceutical and Medicinal Chemistry, University of Tuebingen (Germany)

Glycogen synthase kinase-3 (GSK-3) is known to modulate cell survival and apoptosis through multiple intracellular signaling pathways. However, its hepatoprotective function and its role in activation of NF-{kappa}B and anti-apoptotic factors are poorly understood and remain controversial. Here we investigated whether inhibition of GSK-3 could induce apoptosis in the presence of TNF-{alpha} in primary mouse hepatocytes. We show that pharmacological inhibition of GSK-3 in primary mouse hepatocytes does not lead to TNF-{alpha}-induced apoptosis despite reduced NF-{kappa}B activity. Enhanced stability of I{kappa}B-{alpha} appears to be responsible for lower levels of nuclear NF-{kappa}B and hence reduced transactivation. Additionally, inhibition of GSK-3 was accompanied by marked upregulation of {beta}-catenin, AP-1, and CREB transcription factors. Stimulation of canonical Wnt signaling and CREB activity led to elevated levels of anti-apoptotic factors. Hence, survival of primary mouse hepatocytes may be caused by the activation and/or upregulation of other key regulators of liver homeostasis and regeneration. These signaling molecules may compensate for the compromised anti-apoptotic function of NF-{kappa}B and allow survival of hepatocytes in the presence of TNF-{alpha} and GSK-3 inhibition.

OSTI ID:
21045962
Journal Information:
Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 6 Vol. 314; ISSN 0014-4827; ISSN ECREAL
Country of Publication:
United States
Language:
English

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