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The role of nitric oxide synthase in exercise induced changes in endothelial progenitor cell number
Author(s) -
Colleran Patrick Nicholas,
Tanner Miles A.,
Latcham Shena L.,
Collier Sara L.,
Laughlin M. Harold,
McAllister Richard M.,
Price Elmer M.
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.a750-c
Subject(s) - progenitor cell , nitric oxide synthase , endothelial progenitor cell , endogeny , cd31 , nitric oxide , medicine , endocrinology , cd14 , stem cell , chemistry , angiogenesis , biology , microbiology and biotechnology , receptor
Mobilization of endogenous bone marrow derived endothelial progenitor cells (EPCs) has been shown to play a pivotal role in the neovascularization of adult ischemic tissue, leading to investigation into the potential therapeutic application of these cells in the treatment of cardiovascular disease. Recent work has revealed physical activity to be an effective means of mobilizing endogenous EPCs in a manner dependent on nitric oxide synthase (NOS) enzyme activity. This study was performed to determine the role of NOS enzyme activity in exercise‐induced mobilization of endogenous EPCs. We hypothesized that chronic inhibition of NOS enzyme activity would attenuate exercise‐induced increases in circulating EPC number. Adult male Yucatan swine were exposed to treadmill exercise either in the presence or absence of the nitric oxide synthase inhibitor L‐NAME. Pre‐ and post‐ exercise EPC number was analyzed using fluorescence activated cell sorting (FACS). Chronic blockade of NOS activity had no effect on resting basal CD31 + or CD14 + cell number. In the absence of L‐NAME, exercise produced a 9.2% and a 19.8% increase in CD31 + and CD14 + cell number, respectively. L‐NAME attenuated the exercise‐induced increase in CD31 + cells by 21.9%, a trend approaching statistical significance (P = 0.073), while significantly diminishing the post‐exercise increase in CD14 + cells by 44.7% (P = 0.046). Our data suggest that acute exercise can increase EPCs in a NOS dependent manner. (Supported by NIH grants HL52490, RR188276 and AR048523)