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High glucose-mediated oxidative stress impairs cell migration

Marcelo L Lamers1, Maíra E S Almeida, Miguel Vicente-Manzanares

  • 1Department of Morphological Sciences, Institute of Basic Health Science, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Plos One
|August 10, 2011
PubMed

Insights

High glucose impairs diabetic wound healing by reducing cell migration. This is caused by increased oxidative stress, leading to polarity loss and deficient adhesion, partly due to elevated Rac1 activity.

Area of Science:

  • Cell Biology
  • Diabetic Complications
  • Wound Healing Research

Background:

  • Diabetic patients frequently experience deficient wound healing, with unclear cellular and molecular origins.
  • Understanding the impact of high glucose on cell migration is crucial for addressing this complication.

Purpose of the Study:

  • To investigate the hypothesis that high glucose concentrations inhibit cell migration.
  • To elucidate the cellular and molecular mechanisms underlying impaired cell migration in high glucose conditions.

Main Methods:

  • Cultured various cell types (CHO.K1, NIH-3T3 fibroblasts, MEFs, primary skin fibroblasts) in low glucose (LG), high glucose (HG), or osmotic control (OC) media.
  • Assessed cell migration speed, protrusion stability, polarity, adhesion maturation, and Rac1 activity.
  • Investigated the role of reactive oxygen species (ROS) using N-Acetyl-Cysteine (NAC).

Main Results:

  • High glucose (HG) significantly inhibited cell migration compared to LG and OC conditions.
  • HG-induced inhibition was linked to impaired cell polarity, destabilized protrusions, and reduced adhesion maturation.
  • Increased Rac1 activity in HG conditions promoted protrusion but hindered adhesion maturation, explaining the HG phenotype.
  • N-Acetyl-Cysteine (NAC) partially or fully rescued the effects of HG, indicating a role for oxidative stress.

Conclusions:

  • High glucose impairs cell migration through increased oxidative stress, leading to polarity loss, deficient adhesion, and unstable protrusions.
  • Elevated Rac1 activity is a key factor in mediating these HG-induced cellular alterations.
  • These findings provide mechanistic insights into the poor wound healing observed in diabetic patients.

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