Hypertrophy of cultured adult rat ventricular cardiomyocytes induced by antibodies against the insulin-like growth factor (IGF)-I or the IGF-I receptor is IGF-II-dependent.
作者： Chih‐Yang Huang , Ling‐Yang Hao , Dennis E. Buetow
关键词: Receptor 、 Signal transduction 、 Growth factor 、 Tyrosine kinase 、 Endocrinology 、 Muscle hypertrophy 、 Internal medicine 、 Chemistry 、 Downregulation and upregulation 、 Genistein 、 Insulin-like growth factor
摘要: Antibodies against the insulin-like growth factor-I (IGF-I) or IGF-I receptor (IGF-IR) directly initiate a rapid (within 6 h) hypertrophy of isolated adult rat ventricular cardiomyocytes cultured in absence serum. Further, treated with either these agonistic antibodies upregulate expression their genes for factor-II (IGF-II) and IGF-II (IGF-IIR). Genistein, an inhibitor tyrosine kinase IGF-IR, also induces to hypertrophy. Anti-IGF-II antibody inhibits cardiomyocyte induced by anti-IGF-I anti-IGF-IR genistein. Results are consistent model which local production is upregulated when IGF-IR signaling pathway blocked IGF-II-mediated pathway, likely involving IGF-IIR, then stimulates cardiomyocytes.
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