کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1907558 | 1046378 | 2007 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Evidence against the involvement of nitric oxide in the modulation of telomerase activity or replicative capacity of human endothelial cells
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Evidence against the involvement of nitric oxide in the modulation of telomerase activity or replicative capacity of human endothelial cells Evidence against the involvement of nitric oxide in the modulation of telomerase activity or replicative capacity of human endothelial cells](/preview/png/1907558.png)
چکیده انگلیسی
Telomerase, a reverse transcriptase involved in the maintenance of telomere function and cellular replicative capacity, is thought to be regulated by nitric oxide (NO). Here, we have used pharmacological tools and RNA interference to re-assess the role of NO in the regulation of telomerase and senescence of human umbilical vein endothelial cells. Acute or chronic treatment of these cells with the NO donors diethylenetriamine/NO (DETA-NO) or S-nitroso-N-acetylpenicillamine (SNAP) at concentrations which generated NO in the 1-300Â nM range did not modulate telomerase activity. Similarly these agents did not affect cellular replicative capacity during long-term sub-cultivation. The NO synthase (NOS) inhibitor NG-monomethyl-l-arginine (1Â mM) reduced basal levels of c-GMP by 50% but had no effect on telomerase activity or replicative capacity. Withdrawal of ascorbic acid increased the intracellular pro-oxidant capacity, reduced telomerase activity and increased the accumulation of senescent cells upon serial passage in culture. However, this shift to a more oxidative redox state did not unmask the putative capacity of NO to modulate telomerase or senescence. Infection of cells with a lentiviral vector expressing a small hairpin RNA targeted against endothelial NOS inhibited endogenous NO production completely but failed to affect the decrease of telomerase activity or the accumulation of senescent cells observed with passage in culture. Our findings suggest that physiological concentrations of NO do not modulate telomerase levels or replicative capacity of endothelial cells, regardless of their cellular oxidative status.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Gerontology - Volume 42, Issue 9, September 2007, Pages 904-910
Journal: Experimental Gerontology - Volume 42, Issue 9, September 2007, Pages 904-910
نویسندگان
Ying Hong, Marisol Quintero, Nanci M. Frakich, Elizabeth Trivier, Jorge D. Erusalimsky,