Lack of telomere shortening with age in mouse resting zone chondrocytes

Benjamin U. Nwosu, University of Massachusetts Medical School
Ola Nilsson, National Institutes of Health
Robert D. Mitchum Jr., National Institutes of Health
Marilena Coco, National Institutes of Health
Kevin M. Barnes, National Institutes of Health
Jeffrey Baron, National Institutes of Health

Abstract

BACKGROUND AND AIM: Telomeres are hexameric repeat sequences that flank eukaryotic chromosomes. The telomere hypothesis of cellular aging proposes that replication of normal somatic cells leads to progressive telomere shortening which induces replicative senescence. Previous studies suggest that growth plate chondrocytes have a finite proliferative capacity in vivo. We therefore hypothesized that telomere shortening in resting zone chondrocytes leads to replicative senescence.

METHOD: To test this hypothesis we compared the telomere restriction fragment (TRF) length of Mus casteneus at 1, 4, 8, and 56 weeks of age.

RESULTS AND CONCLUSIONS: We found that TRF length did not diminish measurably with age, suggesting that telomere shortening in resting zone chondrocytes is not the mechanism that limits proliferation of growth plate chondrocytes in vivo.