肌肉肥大
纤维化
生物
肌球蛋白
基因表达
主要组织相容性复合体
体内
转基因小鼠
病理
内科学
转基因
内分泌学
细胞生物学
基因
医学
遗传学
作者
Kumar Pandya,Hyung Suk Kim,Oliver Smithies
标识
DOI:10.1073/pnas.0607700103
摘要
Reexpression of the fetally expressed beta-myosin heavy chain (beta-MHC) gene is a well documented marker of pathological cardiac hypertrophy and normal aging in many experimental models. To gain insights into factors affecting this reexpression of beta-MHC within the complex anatomical structure of the heart, we investigated the spatial pattern of its expression at the level of single cells during aging and hypertrophy. We generated mice that express yellow fluorescent protein fused to the N terminus of the beta-MHC and examined its expression pattern during normal aging and in mice with hypertrophy induced by constitutive expression of a renin transgene. The localization of fibrosis within the hearts also was determined by using a fluorescent lectin. The results show that reexpression of beta-MHC occurs in discrete subsets of myocytes within the subendocardium rather than uniformly throughout the heart, that beta-MHC induction is not an obligatory consequence of cellular hypertrophy, and that beta-MHC-expressing cells in the normal aging heart and the hypertrophic heart are distributed predominantly in clusters within and surrounding foci of fibrosis. We conclude that beta-MHC gene expression in the normal aging adult and hypertrophic mouse heart is a marker of fibrosis rather than of cellular hypertrophy.
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