[Effects of insulin on the distribution of actins in vascular smooth muscle cells in the process of proliferation via mitogen-activated protein kinase in vitro]

Sheng Li Xue Bao. 2002 Apr 25;54(2):165-70.
[Article in Chinese]

Abstract

Proliferation of vascular smooth muscle cells (VSMCs) is often accompanied by changes in intracellular actin distribution. The changes are controlled by the signal transduction pathways of protein kinase C/mitogenic activated protein kinase (PKC-MAPK), but the mechanism is unclear. In order to study the effect of insulin on the intracellular signal transduction (PKC-MAPK) probably involved in the modulation of proliferation and redistribution of actins in the VSMCs, the DNA synthesis, MAPK activities and its gene expression, and the redistribution of intracellular actins were investigated in the isolated VSMCs of SHR pretreated with PKC inhibitor and/or insulin, respectively. We found that insulin treatment resulted in proliferation of the VSMCs and an increase in [(3)H] TdR incorporation. Meanwhile, the activities and expression of MAPK increased significantly compared to the control group. These effects of insulin were blocked by PKC inhibitor. In addition, insulin caused a redistribution of the intracellular actins in VSMCs, which was also inhibited by PKC inhibitor. It is, therefore, suggested that these effects of insulin on VSMCs proliferation and distribution of the intracellular actins may be mediated by the MAPK signal transduction pathway.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Animals
  • Cell Division / drug effects
  • In Vitro Techniques
  • Insulin / pharmacology*
  • Mitogen-Activated Protein Kinases / physiology*
  • Muscle, Smooth, Vascular / cytology*
  • Myocytes, Smooth Muscle / drug effects*
  • Myocytes, Smooth Muscle / enzymology
  • Myocytes, Smooth Muscle / metabolism
  • Protein Kinase C / physiology*
  • Rats
  • Rats, Inbred SHR
  • Tissue Distribution

Substances

  • Actins
  • Insulin
  • Protein Kinase C
  • Mitogen-Activated Protein Kinases