2005 Fiscal Year Final Research Report Summary
Molecular mechanisms underlying exercise training-induced reduction of aortic stiffness
| Project/Area Number |
16500391
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
MAEDA Seiji University of Tsukuba, Graduate School of Comprehensive Human Sciences, Assistant Professor, 大学院・人間総合科学研究科, 講師 (30282346)
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| Co-Investigator(Kenkyū-buntansha) |
IEMITSU Motoyuki University of Tsukuba, Graduate School of Comprehensive Human Sciences, Research Associate, 大学院・人間総合科学研究科, 助手 (90375460)
MIYAUCHI Takashi University of Tsukuba, Graduate School of Comprehensive Human Sciences, Professor, 大学院・人間総合科学研究科, 教授 (60222329)
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| Project Period (FY) |
2004 – 2005
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| Keywords | aorta / exercise training / mRNA / vasoactive factor / arterial stiffness / heart |
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| Research Abstract |
Regular aerobic exercise reduces aortic stiffness. However, the mechanisms by which chronic exercise lowers arterial stiffness are not known. To determine the molecular mechanisms of these changes, the alteration of gene expression in the aorta by aerobic exercise training was measured with the microarray technique. The differences in expression levels of 3,800 genes in the abdominal aorta of sedentary control (8 weeks old) and exercise-trained rats (8 weeks old, treadmill running for 4 weeks) were compared by the microarray analysis. Aortic pulse wave velocity (PWV) was lower and systemic arterial compliance was higher (both P<0.05) in the exercise-trained group than in the control group. Of the 323 genes that displayed differential expression (upregulation of 206 genes and downregulation of 117 genes), a total of 29 genes (24 upregulated and 5 downregulated genes) were identified as potential candidate genes that may be involved in vasodilation and arterial destiffening. Using real-time quantitative PCR, we confirmed the results of microarray analysis that prostaglandin EP2 receptor (PGE-EP2R), prostaglandin EP4 receptor (PGE-EP4R), C-type natriuretic peptide (CNP), and endothelial nitric oxide synthase (eNOS) genes were differentially expressed. Furthermore, there were modest correlations between arterial stiffness and levels of these factors. Differential expression of eNOS gene was further verified at protein level by using Western blot analysis. These results suggest that exercise training induces the altered expression in several genes including prostaglandin, CNP, and nitric oxide in the aorta and that these molecular changes (particularly eNOS as its protein expression was altered) may contribute, at least in part, to the beneficial effect of exercise training on aortic stiffness.
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