Expression of Follistatin-Related Genes Is Altered in Heart Failure

卵泡抑素 心力衰竭 心肌细胞 川地31 生物 内皮 内科学 细胞外基质 基因表达 炎症 内分泌学 细胞生物学 免疫组织化学 医学 基因 遗传学
作者
Enrique Lara‐Pezzi,Leanne E. Felkin,Emma J. Birks,Padmini Sarathchandra,Kalyani D. Panse,Robert S. George,Jennifer L. Hall,Magdi H. Yacoub,Nadia Rosenthal,Paul J.R. Barton
出处
期刊:Endocrinology [The Endocrine Society]
卷期号:149 (11): 5822-5827 被引量:89
标识
DOI:10.1210/en.2008-0151
摘要

Follistatins play roles in diverse biological processes including cell proliferation, wound healing, inflammation, and skeletal muscle growth, yet their role in the heart is currently unknown. We have investigated the myocardial expression profile and cellular distribution of follistatin (FST) and the FST-like genes FSTL1 and FSTL3 in the normal and failing heart. Expression was further analyzed in the novel setting of recovery from heart failure in myocardium obtained from patients who received combined mechanical (left ventricular assist device) and pharmacological therapy. Real-time PCR revealed that FSTL1 and FSTL3 expression was elevated in heart failure but returned to normal after recovery. FSTL3 expression levels correlated with molecular markers of disease severity and FSTL1 with the endothelial cell marker CD31, suggesting a potential link with vascularization. FSTL1 levels before treatment correlated with cardiac function after recovery, suggesting initial levels may influence long-term outcome. Immunohistochemistry revealed that FST was primarily localized to fibroblasts and vascular endothelium within the heart, whereas FSTL1 was localized to myocytes, endothelium, and smooth muscle cells and FSLT3 to myocytes and endothelium. Microarray analysis revealed that FST and FSTL1 were associated with extracellular matrix-related and calcium-binding proteins, whereas FSTL3 was associated mainly with cell signaling and transcription. These data show for the first time that elevated myocardial expression of FST-like genes is a feature of heart failure and may be linked to both disease severity and mechanisms underlying recovery, revealing new insight into the pathogenesis of heart failure and offering novel therapeutic targets.
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