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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Macrophage-induced preadipocyte survival depends on signaling through Akt, ERK1/2, and reactive oxygen species

André S D Molgat1, AnneMarie Gagnon, Alexander Sorisky

  • 1Chronic Disease Program, Ottawa Hospital Research Institute, Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada.

Experimental Cell Research
|November 9, 2010
PubMed

Insights

Macrophage-conditioned medium (MacCM) promotes preadipocyte survival through Akt and ERK1/2 signaling pathways. This process requires reactive oxygen species (ROS) generation, highlighting a novel mechanism in adipose tissue remodeling.

Area of Science:

  • Cell Biology
  • Metabolic Research
  • Immunology

Background:

  • Obesity involves adipose tissue remodeling, including macrophage infiltration and adipocyte changes.
  • Previous work showed macrophage-conditioned medium (MacCM) protects preadipocytes from apoptosis via platelet-derived growth factor (PDGF).

Purpose of the Study:

  • Investigate intracellular signaling pathways activated by MacCM and PDGF in preadipocyte survival.
  • Determine the role of reactive oxygen species (ROS) in MacCM-induced pro-survival signaling.

Main Methods:

  • Stimulation of 3T3-L1 preadipocytes with J774A.1-MacCM or PDGF.
  • Inhibition of phosphoinositide 3-kinase (PI3K) and MEK1/2 pathways.
  • Measurement of Akt and ERK1/2 phosphorylation.
  • Assessment of reactive oxygen species (ROS) levels using diphenyleneiodonium (DPI) and N-acetyl cysteine (NAC).

Main Results:

  • MacCM and PDGF strongly stimulated Akt and ERK1/2 phosphorylation.
  • Inhibiting PI3K or MEK1/2 abrogated phosphorylation and impaired pro-survival effects.
  • MacCM increased ROS levels, which was essential for Akt/ERK1/2 signaling and preadipocyte survival.
  • Serum withdrawal also increased ROS, and DPI/NAC attenuated cell death.

Conclusions:

  • MacCM-dependent 3T3-L1 preadipocyte survival relies on Akt and ERK1/2 signaling.
  • ROS generation by MacCM is crucial for activating these pathways and promoting survival.
  • These findings suggest mechanisms by which macrophages influence adipocyte fate in obesity.

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