Vascular endothelial cell senescence mediated by integrin beta4 in vitro

FEBS Lett. 2007 Nov 27;581(28):5337-42. doi: 10.1016/j.febslet.2007.10.027. Epub 2007 Oct 25.

Abstract

To understand whether integrin beta4 is involved in vascular endothelial cell (VEC) senescence, we examined integrin beta4 level changes, as well as P53 and reactive oxygen species (ROS) levels and alterations of phosphatidylcholine-specific phospholipase C (PC-PLC) activity before and after knocking-down integrin beta4 by small interfering RNA. We found integrin beta4, P53 and ROS levels increased significantly, while Ca(2+)-independent PC-PLC activity obviously decreased during VEC senescence. On the other hand, integrin beta4 down-regulation attenuated the senescence phenotype and reversed Ca(2+)-independent PC-PLC activity, and P53 and ROS levels. The data suggested that integrin beta4 might mediate VEC senescence through depressing Ca(2+)-independent PC-PLC and elevating the levels of P53 and ROS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcium / pharmacology
  • Cells, Cultured
  • Cellular Senescence / physiology*
  • Down-Regulation
  • Endothelial Cells / metabolism*
  • Enzyme Activation / drug effects
  • Humans
  • Integrin beta4 / genetics
  • Integrin beta4 / metabolism*
  • RNA, Small Interfering / genetics
  • Reactive Oxygen Species / metabolism
  • Tumor Suppressor Protein p53 / metabolism
  • Type C Phospholipases / metabolism

Substances

  • Integrin beta4
  • RNA, Small Interfering
  • Reactive Oxygen Species
  • Tumor Suppressor Protein p53
  • Type C Phospholipases
  • phosphatidylcholine-specific phospholipase C
  • Calcium