Lack of Replicative Senescence in Normal Rodent Glia

• Published in: Science (American Association for the Advancement of Science) Vol. 291; no. 5505; pp. 872 - 875
• Main Authors: Mathon, Nicole F., Malcolm, Denise S., Harrisingh, Marie C., Cheng, Lili, Lloyd, Alison C.
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society for the Advancement of Science 02.02.2001; American Association for the Advancement of Science; The American Association for the Advancement of Science
• Subjects: Aging; Anatomy; Animals; beta-Galactosidase - metabolism; Biological and medical sciences; Blood; Carrier Proteins - metabolism; Cell aging; Cell Culture Techniques; Cell cycle; Cell cycle, cell proliferation; Cell Division; Cell growth; Cell Line; Cell lines; Cell physiology; Cell Size; Cells; Cells, Cultured; Cellular biology; Cellular Senescence; Clone Cells; Culture Conflict; Culture Media; Cultured cells; Cyclin-Dependent Kinase Inhibitor p16; Cyclin-Dependent Kinases - metabolism; Cyclins - metabolism; Fibroblasts; Fibroblasts - cytology; Fibroblasts - physiology; Fundamental and applied biological sciences. Psychology; Genetic aspects; Genetic research; Giant cells; Giant Cells - cytology; Glia; Logical Thinking; Molecular and cellular biology; Mutation; Neuroglia; Phenotype; Proteins - metabolism; ras Proteins - metabolism; Rats; Rattus; Rodents; Schwann cells; Schwann Cells - cytology; Schwann Cells - physiology; Somatic cells; Telomerase - metabolism; Telomere - physiology; Tumor Suppressor Protein p14ARF; Tumor Suppressor Protein p53 - metabolism; United States; Cell proliferation; Vertebrata; Senescence; Mammalia; Cell line; Mouse; Rodentia; Replication
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.1056782

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.