Lack of replicative senescence in normal rodent glia

Science. 2001 Feb 2;291(5505):872-5. doi: 10.1126/science.1056782. Epub 2001 Jan 18.

Abstract

Replicative senescence is thought to be an intrinsic mechanism for limiting the proliferative life-span of normal somatic cells. We show here that rat Schwann cells can be expanded indefinitely in culture while maintaining checkpoints normally lost during the immortalization process. These findings demonstrate that senescence is not an inevitable consequence of extended proliferation in culture.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood
  • Carrier Proteins / metabolism
  • Cell Culture Techniques
  • Cell Division*
  • Cell Line
  • Cell Size
  • Cells, Cultured
  • Cellular Senescence*
  • Clone Cells
  • Culture Media
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinases / metabolism
  • Cyclins / metabolism
  • Fibroblasts / cytology
  • Fibroblasts / physiology
  • Giant Cells / cytology
  • Mutation
  • Phenotype
  • Proteins / metabolism
  • Rats
  • Schwann Cells / cytology*
  • Schwann Cells / physiology
  • Telomerase / metabolism
  • Telomere / physiology
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53 / metabolism
  • beta-Galactosidase / metabolism
  • ras Proteins / metabolism

Substances

  • Carrier Proteins
  • Culture Media
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclins
  • Proteins
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53
  • Cyclin-Dependent Kinases
  • Telomerase
  • beta-Galactosidase
  • ras Proteins