Mild heat shock induces cyclin D1 synthesis through multiple Ras signal pathways

FEBS Lett. 2002 Mar 27;515(1-3):141-5. doi: 10.1016/s0014-5793(02)02459-6.

Abstract

Hyperthermia such as that occurring during fever may improve cell survival during infection, although its mechanism of action is largely unknown. Here we show that acute exposure to mild, but not severe, heat shock induces the synthesis of cyclin D1 that plays a critical role(s) in G1 progression of the cell cycle. This induction seemed to be regulated through multiple Ras signal pathways involving extracellular signal-regulated kinase, phosphatidylinositol 3-kinase, and Rac1/NADPH oxidase, all of which have well been documented to be responsible for growth factor-induced cyclin D1 expression. In a physiological sense, mild heat shock may regulate cell proliferation through inducing cyclin D1 along with growth factors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle / physiology
  • Cell Division / physiology
  • Cell Line
  • Cyclin D1 / biosynthesis*
  • Enzyme Inhibitors / pharmacology
  • Fever / metabolism
  • Fibroblasts / cytology
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Heat-Shock Response / physiology*
  • Humans
  • Mice
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism
  • NADPH Oxidases / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Rats
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • rac1 GTP-Binding Protein / genetics
  • rac1 GTP-Binding Protein / metabolism
  • ras Proteins / metabolism*

Substances

  • Enzyme Inhibitors
  • Cyclin D1
  • NADPH Oxidases
  • Phosphatidylinositol 3-Kinases
  • Mitogen-Activated Protein Kinases
  • rac1 GTP-Binding Protein
  • ras Proteins