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Sirt1 increases satellite cell cycle progression
Author(s) -
Rathbone Chris Ronald,
Lees Simon James,
Booth Frank
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1426
Subject(s) - cell cycle , biology , cyclin b1 , cyclin dependent kinase , retinoblastoma protein , microbiology and biotechnology , cell growth , cyclin , cell , cancer research , cyclin dependent kinase 1 , biochemistry
The repair, regrowth, and hypertrophy of skeletal muscle is largely dependent on the proliferation of satellite cells, muscle precursor cells located between the basal lamina and plasmalemma of mature muscle fibers. The objective of the present study was to determine the effect of the class III, NAD+‐dependent histone deacetylase, Sirt1, on satellite cell cycle progression. Satellite cells were isolated from Fischer 344 × Brown Norway F1 hybrid male rats (3–4 months old), cultured for 5–6 days, passagedonce, and seeded onto Matrigel‐coated tissue culture plates. 18 hours later, cells were infected with a recombinant adenovirus engineered to overexpress Sirt1 (Ad‐Sirt1) or β‐galactosidase (Ad‐LacZ) to determine the effects of increasing Sirt1 on satellite cell cycle progression. Ad‐Sirt1 infection increased MPC cell cycle progression and markers of the proliferative state as evidenced by an increase in cell number, PCNA expression, and the phosphorylation of retinoblastoma protein. Ad‐Sirt1 infection decreased and increased the expression of the cyclin dependent kinase inhibitors p21 Waf/Cip1 and p27 Kip1 , respectively. These studies identify Sirt1 as a positive regulator of MPC cycle progression, potentially through its ability to decrease the levels of the cdk inhibitor p21 Waf/Cip1 . Supported by NIH AG18780 and NIH AR048523