Superoxide-mediated actin response in post-hypoxic endothelial cells. Academic Article uri icon

Overview

MeSH

  • Animals
  • Cattle
  • Cell Movement
  • Humans
  • Neovascularization, Physiologic
  • Phosphorylation
  • Superoxide Dismutase

MeSH Major

  • Actins
  • Cell Hypoxia
  • Endothelium, Vascular
  • Superoxides

abstract

  • The mechanism leading to changes in the superstructure of endothelial cells exposed to ischemia and reperfusion remains uncharacterized. We show that in post-hypoxic endothelial cells, the simple re-addition of oxygen induces a profound reorganization of the actin cytoskeleton. The total filamentous actin pool increases by 41% and translocation of actin filaments to the submembranous network is observed. Concurrent with the actin polymerization, increased tyrosine phosphorylation of endothelial cell substrates is detected on Western blots. Overexpression of superoxide dismutase using replication incompetent adenovirus inhibits the actin and tyrosine phosphorylation responses to reoxygenation. Inhibition of tyrosine kinases with the isoflavone genistein also suppressed the actin polymerization response to reoxygenation, but unlike superoxide dismutase, genistein also induced the collapse of the superstructure of endothelial cells upon reoxygenation. These experiments support the concept that reoxygenation following a period of hypoxia can induce the remodeling of the actin cytoskeleton in endothelial cells. Such a response requires the intact coupling of superoxide producing pathway(s) with tyrosine kinase pathway(s).

publication date

  • October 25, 1996

has subject area

  • Actins
  • Animals
  • Cattle
  • Cell Hypoxia
  • Cell Movement
  • Endothelium, Vascular
  • Humans
  • Neovascularization, Physiologic
  • Phosphorylation
  • Superoxide Dismutase
  • Superoxides

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 8900169

Additional Document Info

start page

  • 26863

end page

  • 26867

volume

  • 271

number

  • 43