Premium
miRNA‐21 and miRNA‐133b are decreased in hyperthyroidism‐induced cardiac hypertrophy – Critical role of Type 1 Angiotensin II receptor (AT1R)
Author(s) -
Diniz Gabriela Placoná,
Takano Ana Paula C,
BarretoChaves Maria Luiza Morais
Publication year - 2013
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.27.1_supplement.737.1
Subject(s) - losartan , medicine , endocrinology , muscle hypertrophy , microrna , angiotensin ii , renin–angiotensin system , receptor , biology , blood pressure , gene , biochemistry
Objective To investigate the miRNA‐21 and miRNA‐133b levels in T4‐induced cardiac hypertrophy, as well as the potential influence exerted by AT1R in this response. Hyperthyroidism was induced by daily intraperitoneal injections of 0.100 mg/kg of T4 for 14 days. The T4 group was then subdivided into two groups: T4 and T4 plus Losartan, which was administrated in the drinking water once a day for 14 days (200mg/L). The analysis of miRNA expression was assessed by MicroRNA Stem Loop RT‐PCR. Results Cardiac hypertrophy in T4 group confirmed by the higher heart weight, heart weight to tibia length ratio, as well as by the increase of ANF and skeletal‐alpha actin levels, was prevented by Losartan. In addition, T4‐induced cardiac hypertrophy was accompanied by decreased miRNA‐21 and miRNA‐133b levels (P<0.01, vs control). However, the AT1R inhibitor blocked the reduction of miRNA‐21, as well as attenuated the reduction of miRNA‐133b promoted by T4. Conclusions Considering that increased miRNA‐133b was able to prevent the cardiac hypertrophy development, and that miRNA‐21 inhibition promoted cardiac growth, it is possible that the modulation of these miRNAs may exert an important role to the cardiac hypertrophy development induced by T4, as well as to the prevention of the cardiac growth evidenced by the AT1R blockade. Research support: Supported by Foundation for the Support of Research in the State of São Paulo.