Regulation of endothelial cell morphogenesis by the protein kinase D (PKD)/glycogen synthase kinase 3 (GSK3)β pathway

Am J Physiol Cell Physiol. 2012 Oct 1;303(7):C743-56. doi: 10.1152/ajpcell.00442.2011. Epub 2012 Aug 1.

Abstract

Vascular morphogenesis is a key process for development, reproduction, and pathogenesis. Thus understanding the mechanisms of this process is of pathophysiological importance. Despite the fact that collagen I is the most abundant and potent promorphogenic molecule known, the molecular mechanisms by which this protein regulates endothelial cell tube morphogenesis are still unclear. Here we provide strong evidence that collagen I induces tube morphogenesis by inhibiting glycogen synthase kinase 3β (GSK3β). Further mechanistic studies revealed that GSK3β activity is regulated by protein kinase D (PKD). PKD inhibited GSK3β activity, which was required for collagen I-induced endothelial tube morphogenesis. We also found that GSK3β regulated trafficking of integrin α(2)β(1) in a Rab11-dependent manner. Taken together, our studies highlight the important role of PKD in the regulation of collagen I-induced vascular morphogenesis and show that it is mediated by the modulation of GSK3β activity and integrin α(2)β(1) trafficking.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Endothelial Cells / enzymology*
  • Glycogen Synthase Kinase 3 / physiology*
  • Glycogen Synthase Kinase 3 beta
  • HEK293 Cells
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Integrin alpha2beta1 / physiology*
  • Morphogenesis / physiology*
  • Protein Kinase C / physiology*
  • Protein Transport / physiology
  • Signal Transduction

Substances

  • Integrin alpha2beta1
  • protein kinase D
  • GSK3B protein, human
  • Glycogen Synthase Kinase 3 beta
  • Protein Kinase C
  • Glycogen Synthase Kinase 3