Testosterone in aging cardiac cells and the role of cell cycle regulation factors.docVIP

 PAGE \* MERGEFORMAT 17 Testosterone in aging cardiac cells and the role of cell cycle regulation factors [Abstract] Objective To investigate the myocardial cells of different doses of testosterone on the intervention of aging and its possible mechanism. Methods 1 μ mol / L, 100 nmol / L, 10 nmol / L dose of testosterone, three kinds of intervention in the natural aging mouse cardiac cells detected by flow cytometry cell cycle distribution of each group, with RT  PCR and Western blot analysis of various group of cells, p16INK4a, cyclinD1 mRNA, protein and dephosphorylated RB protein expression. The results, compared with the aging cardiac myocytes, 1 μ mol / L, 100 nmol / L, 10 nmol / L testosterone interfere with the proportion of cells in G0/G1 phase decreased significantly (P amp;lt;0.05), this role has a dose-dependent. Testosterone intervention can increase cyclinD1mRNA and protein expression, down p16INK4a mRNA and protein expression, and to dephosphorylated RB protein expression decreased (P amp;lt;0.05), but these effects may be androgen receptor antagonist and not be affected by estrogen blocked by blocker (P amp;lt;0.05). Conclusion Testosterone dose-dependent inhibition of mouse cardiac cell senescence, the role of testosterone increase cyclinD1 in part by the expression of p16INK4a and reduced dephosphorylated RB protein expression achieved. Effect of testosterone on aging myocardial cell and the cell cycle regulation XING Xiao  Wen, WU Sai  Zhu, RUAN Yun  Jun, et al. Department of Cardiology, Nanfang Hospital, Nanfang Medical University, Guangzhou 510515, Guangdong, China [Abstract] Objective To investigate the effect of testosterone on the aging myocardial cell and the possible mechanism. Methods 1 μ mol / L, 100 and 10 nmol / L testosterone were administrated on natural aging murine myocardial cells, and the distribution of cell cycle was measured by flow cytometry. p16INK4a, cyclinD1 mRNA and protein and dephosphorylation RB protein