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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Aerobic Exercise Training-Induced Left Ventricular Hypertrophy Involves Regulatory MicroRNAs, Decreased Angiotensin-Converting Enzyme-Angiotensin II, and Synergistic Regulation of Angiotensin-Converting Enzyme 2-Angiotensin (1-7)

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Author(s):
Fernandes, Tiago [1] ; Hashimoto, Nara Y. [1] ; Magalhaes, Flavio C. [1] ; Fernandes, Fernanda B. [2] ; Casarini, Dulce E. [2] ; Carmona, Adriana K. [3] ; Krieger, Jose E. [4] ; Phillips, M. Ian [5] ; Oliveira, Edilamar M. [1, 5]
Total Authors: 9
Affiliation:
[1] Univ Sao Paulo, Sch Phys Educ & Sport, Lab Biochem & Mol Biol Exercise, BR-05508900 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Div Nephrol, Kidney & Hypertens Hosp, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Biophys, Sao Paulo - Brazil
[4] Univ Sao Paulo, Sch Med, InCor, Lab Genet & Mol Cardiol, BR-05508900 Sao Paulo - Brazil
[5] Keck Grad Inst, Lab Stem Cells, Claremont, CA - USA
Total Affiliations: 5
Document type: Journal article
Source: Hypertension; v. 58, n. 2, p. 182-U121, AUG 2011.
Web of Science Citations: 102
Abstract

Aerobic exercise training leads to a physiological, nonpathological left ventricular hypertrophy; however, the underlying biochemical and molecular mechanisms of physiological left ventricular hypertrophy are unknown. The role of microRNAs regulating the classic and the novel cardiac renin-angiotensin (Ang) system was studied in trained rats assigned to 3 groups: (1) sedentary; (2) swimming trained with protocol 1 (T1, moderate-volume training); and (3) protocol 2 (T2, high-volume training). Cardiac Ang I levels, Ang-converting enzyme (ACE) activity, and protein expression, as well as Ang II levels, were lower in T1 and T2; however, Ang II type 1 receptor mRNA levels (69% in T1 and 99% in T2) and protein expression (240% in T1 and 300% in T2) increased after training. Ang II type 2 receptor mRNA levels (220%) and protein expression (332%) were shown to be increased in T2. In addition, T1 and T2 were shown to increase ACE2 activity and protein expression and Ang (1-7) levels in the heart. Exercise increased microRNA-27a and 27b, targeting ACE and decreasing microRNA-143 targeting ACE2 in the heart. Left ventricular hypertrophy induced by aerobic training involves microRNA regulation and an increase in cardiac Ang II type 1 receptor without the participation of Ang II. Parallel to this, an increase in ACE2, Ang (1-7), and Ang II type 2 receptor in the heart by exercise suggests that this nonclassic cardiac renin-angiotensin system counteracts the classic cardiac renin-angiotensin system. These findings are consistent with a model in which exercise may induce left ventricular hypertrophy, at least in part, altering the expression of specific microRNAs targeting renin-angiotensin system genes. Together these effects might provide the additional aerobic capacity required by the exercised heart. (Hypertension. 2011;58:182-189.). (AU)