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A distinct AMP‐activated protein kinase phosphorylation site characterizes cardiac hypertrophy induced by l ‐thyroxine and angiotensin II
Author(s) -
Jiang ShengYang,
Xu Ming,
Ma XiaoWei,
Xiao Han,
Zhang YouYi
Publication year - 2010
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2010.05404.x
Subject(s) - ampk , phosphorylation , medicine , endocrinology , angiotensin ii , amp activated protein kinase , protein kinase a , muscle hypertrophy , kinase , chemistry , knockout mouse , biology , biochemistry , receptor
Summary 1. The purpose of the present study was to evaluate differences in the AMP‐activated protein kinase (AMPK) phosphorylation sites in cardiac hypertrophy induced by l ‐thyroxine and angiotensin (Ang) II. 2. Cardiac hypertrophy was induced in wild‐type and AMPKα2‐knockout mice by treatment with 1 mg/kg, i.p., thyroxine or 1.44 mg/kg per day AngII for 14 days. The phenotype of the hypertrophy was evaluated using echocardiographic measurments and histological analyses. The phosphorylation of AMPK at α‐Ser 485/491 and α‐Thr 172 was determined by western blot analysis. 3. In wild‐type mice, the phosphorylation of AMPKα‐Ser 485/491 was significantly elevated in the AngII‐treated group, but not in the thyroxine‐reated group, compared with the vehicle control group. In contrast, the phosphorylation of AMPKα‐Thr 172 was significantly increased by thyroxine, but not AngII, treatment compared with the vehicle control group. Furthermore, knockout of the AMPKα2 subunit abolished phosphorylation at the α‐Ser 485/491 site and significantly suppressed phosphorylation at the α‐Thr 172 site, resulting in alleviation of thyroxine‐ but not AngII‐induced hypertrophy. 4. In conclusion, l ‐thyroxine and AngII induce the phosphorylation of distinct sites of AMPK in cardiac hypertrophy. Phosphorylation of AMPK α‐Thr 172 may contribute to thyroxine‐induced cardiac hypertrophy.