High glucose inhibits apoptosis in human coronary artery smooth muscle cells by increasing bcl-xL and bfl-1/A1

Am J Physiol Cell Physiol. 2002 Aug;283(2):C422-8. doi: 10.1152/ajpcell.00577.2001.

Abstract

Cardiovascular disease is a serious complication in diabetic patients. To elucidate the precise mechanisms of atherosclerosis in diabetic patients, the effects of high glucose concentration (25 mM) on apoptosis regulation and bcl-2 family protein expression in human coronary artery smooth muscle cells (CASMC) were examined. Treatment with a high level of glucose (25 mM) caused a significant decrease in apoptosis in CASMC compared with the same cells treated with a physiologically normal glucose concentration (5.5 mM) (23.9 +/- 2.4% vs. 16.5 +/- 1.8%; P < 0.01). With respect to apoptosis regulation, treatment of CASMC with high glucose concentration markedly increased mRNA expressions of bcl-xL and bfl-1/A1 compared with cells treated with normal glucose. High glucose induced phosphorylation of phosphatidylinositol 3-kinase (PI 3-K) and extracellular signal-regulated kinase (ERK)1/2 along with bcl-xL and bfl-1/A1 upregulation. These results suggest that high glucose suppresses apoptosis via upregulation of bcl-xL and bfl-1/A1 levels through PI 3-K and ERK1/2 pathways in CASMC. High glucose-induced increase in the expression of antiapoptotic proteins may be important in the development of atherosclerosis in diabetic patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Arteries / cytology
  • Arteries / drug effects
  • Arteries / physiology
  • Cells, Cultured
  • Coronary Vessels / cytology
  • Coronary Vessels / drug effects
  • Coronary Vessels / physiology*
  • Dose-Response Relationship, Drug
  • Enzyme Activation
  • Glucose / administration & dosage*
  • Glucose / pharmacology
  • Humans
  • Minor Histocompatibility Antigens
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / metabolism
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / physiology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Up-Regulation
  • bcl-X Protein

Substances

  • BCL2-related protein A1
  • BCL2L1 protein, human
  • Minor Histocompatibility Antigens
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-X Protein
  • Phosphatidylinositol 3-Kinases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • Glucose