Advanced search
Start date
Betweenand
(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)

Full text
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)