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NO deficiency enhances age‐dependent decline in telomerase activity in mesenteric arteries. A gender‐dependent response
Author(s) -
Wu Licheng,
Huang An,
Kaley Gabor,
Sun Dong
Publication year - 2006
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.20.4.a314-b
Subject(s) - telomerase , telomere , enos , mesenteric arteries , medicine , endocrinology , biology , knockout mouse , nitric oxide , artery , nitric oxide synthase , genetics , dna , gene , receptor
The purpose of the present study was to investigate the effect of NO deficiency on telomerase activity (TA) and telomere length (TL) in mesenteric arteries of 6, 14 and 24‐month‐old male and female eNOS knockout (KO) and wild type (WT) mice. TA and TL were assessed by the Telo TAGGG Telomerase PCR ELISA PLUS kit and Telo TAGGG Telomere Length Assay kit (Roche). We found that aging continuously and significantly decreased TA. Compared to vessels of 6‐month‐old mice, TA in vessels of 24‐month‐old mice decreased by 54 to 75%. There were significant differences in TA between vessels of male and female mice. For example, the optical densities of TA in vessels of 6, 14 and 24‐month female WT mice were 0.50, 0.36 and 0.22, whereas in corresponding vessels of male WT mice they were only 0.38, 0.21 and 0.12, respectively. NO deficiency had no significant effect on TA in female vessels, but it significantly decreased TA in male vessels. For example, TA in vessels of 6‐ and 24‐month male KO mice was only 0.31 and 0.08, values which are significantly less than those in corresponding WT vessels. TL in mesenteric arteries was 64 – 80 Kb. There were no significant differences in TL among the groups. We conclude that telomerase activity is mainly influenced by the aging process. Female hormones and/or genetic encoding provide a significant protection of telomerase activity in female vessels. Nitric oxide, derived from eNOS, plays a significant role in the maintenance of telomerase activity in vessels of male mice. (Supported by NIH grants HL‐43023, HL‐68813 and HL‐070653)