Abstract:
:Our previous studies showed that homocysteine (Hcy) reduces endothelial progenitor cell (EPC) numbers and impairs functional activity. However, the mechanisms by which Hcy reduces EPCs numbers and activity remain to be determined. Recent studies have demonstrated that reduced EPCs numbers and activity was associated with EPCs senescence which involved telomerase activity. Therefore, we investigated whether Hcy accelerates the onset of EPCs senescence through telomerase inactivation, leading to cellular dysfunction. EPCs were isolated from peripheral blood and characterized. After ex vivo cultivation, EPCs became senescent as determined by acidic beta-galactosidase staining. Hcy dose-dependently accelerated the onset of EPCs senescence in culture. Moreover, Hcy decreased proliferation of EPCs as assessed by BrdU incorporation assay and colony-forming capacity. To get further insights into the underlying mechanisms of these effects induced by Hcy, we measured telomerase activity and determined the phosphorylation of Akt by using western blot. Hcy significantly diminished telomerase activity and Akt phosphorylation. Taken together, the results of the present study demonstrated that Hcy accelerated the onset of EPCs senescence, leading to cellular dysfunction. The effect of Hcy might be dependent on telomerase inactivation, and Akt dephosphorylation also appeared to play a major role. In addition, atorvastatin had a preventative effect against Hcy-induced EPCs senescence.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Zhu JH,Chen JZ,Wang XX,Xie XD,Sun J,Zhang FRdoi
10.1016/j.yjmcc.2006.01.011subject
Has Abstractpub_date
2006-05-01 00:00:00pages
648-52issue
5eissn
0022-2828issn
1095-8584pii
S0022-2828(06)00022-8journal_volume
40pub_type
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journal_title:Journal of molecular and cellular cardiology
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journal_title:Journal of molecular and cellular cardiology
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