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Gas6-axl receptor signaling is regulated by glucose in vascular smooth muscle cells

Megan E Cavet1, Elaine M Smolock, Oktay H Ozturk

  • 1Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|February 23, 2008
PubMed
Abstract

Insights

Glucose levels significantly impact Axl signaling in vascular smooth muscle cells (VSMCs). This study reveals how glucose concentration alters Axl

Area of Science:

  • Biochemistry
  • Cell Biology
  • Diabetic Complications

Background:

  • The receptor tyrosine kinase Axl and its ligand Gas6 play roles in diabetic kidney disease.
  • Axl activation by reactive oxygen species in vascular smooth muscle cells (VSMCs) promotes migration and survival, indicating involvement in diabetic vascular complications.

Purpose of the Study:

  • To investigate how varying glucose concentrations affect Axl signaling pathways in VSMCs.
  • To elucidate the mechanism by which Axl contributes to VSMC dysfunction in diabetes.

Main Methods:

  • Examined the impact of different glucose concentrations on Gas6-Axl signaling in VSMCs.
  • Utilized co-immunoprecipitation to analyze Axl's interaction with binding partners under varying glucose conditions.
  • Assessed the effects of glucose on Akt, mTOR, and ERK1/2 activation.

Main Results:

  • Glucose significantly modulated Gas6-Axl signaling: low glucose enhanced Akt and mTOR activation, while high glucose favored ERK1/2 activation.
  • Glucose altered Axl's binding partners: increased association with PI3-kinase p85 subunit in low glucose and with SHP-2 in high glucose.
  • Gas6-Axl-mediated cell migration was higher in high glucose, whereas apoptosis inhibition was more pronounced in low glucose.

Conclusions:

  • Glucose concentration differentially regulates Axl signaling by modulating its interactions with specific binding partners.
  • This study provides a mechanism for Axl's contribution to VSMC dysfunction in the context of diabetes.

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