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Melanocortin-4 receptor-mediated inhibition of apoptosis in immortalized hypothalamic neurons via mitogen-activated

Biaoxin Chai1, Ji-Yao Li, Weizhen Zhang

  • 1Department of Surgery, University of Michigan, Ann Arbor, MI, USA.

Peptides
|June 30, 2006
PubMed

Insights

Melanocortin-4 receptor (MC4R) activation in GT1-1 cells inhibits apoptosis. This effect is mediated by ERK1/2 phosphorylation, suggesting MC4R signaling plays a role in cell survival.

Area of Science:

  • Neuroendocrinology
  • Cell Signaling
  • Molecular Biology

Background:

  • The melanocortin-4 receptor (MC4R) is a G protein-coupled receptor involved in various physiological processes.
  • The GT1-1 cell line expresses endogenous MC4R, making it a suitable model for studying its function.

Purpose of the Study:

  • To investigate MC4R signaling pathways in GT1-1 cells.
  • To determine the effect of the MC4R agonist NDP-MSH on apoptosis in GT1-1 cells.

Main Methods:

  • RT-PCR was used to confirm MC4R mRNA expression.
  • Functional receptor activity was assessed by NDP-MSH binding and cAMP production.
  • Apoptosis was induced by serum deprivation and modulated by NDP-MSH, SHU9119 (antagonist), and PD98059 (MAPK inhibitor).
  • ERK1/2 phosphorylation was measured as a downstream signaling event.

Main Results:

  • MC4R mRNA and functional expression were confirmed in GT1-1 cells.
  • NDP-MSH stimulated GnRH release and inhibited serum deprivation-induced apoptosis.
  • The antiapoptotic effect of NDP-MSH was blocked by SHU9119 and PD98059.
  • NDP-MSH induced dose-dependent ERK1/2 phosphorylation, which was inhibited by SHU9119.

Conclusions:

  • MC4R activation in GT1-1 cells leads to ERK1/2 phosphorylation.
  • MC4R signaling is associated with antiapoptotic effects in these cells, mediated via the MAP kinase pathway.

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