Embryonic Smooth Muscle Myosin Heavy Chain SMemb is Expressed in Pressure-Overloaded Cardiac Fibroblasts
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概要
- 論文の詳細を見る
Left ventricular hypertrophy (LVH) is a secondary adaptation to increased external load. Various qualitative and quantitative changes in myocytes and extracellular components occur during the development of LVH. It has recently been demonstrated that α-smooth muscle actin (α-SMA)-expressing myofibroblasts appear in the interstitium of the heart subjected to increased workload suggesting that cardiac fibroblasts as well as myocytes alter their phenotype in response to pressure overload. In the present study, to explore the load-induced response and phenotypic modulation of cardiac fibroblasts, the localization of embryonic smooth muscle myosin heavy chain (SMemb) and α-SMA in thoracic aorta-constricted rat hearts was investigated by immunohistochemistry, and the morphology of the SMemb-expressing cells was examined by electron microscopy. In addition, to clarify the mechanisms by which SMemb is induced in pressure-overloaded hearts, mRNA expression of SMemb in aorta-constricted rat hearts and in transforming growth factor-β1 (TGF-β1)-treated or mechanically-stretched cultured cardiac fibroblasts was investigated. Enhanced staining of SMemb and α-SMA was detected in the interstitial spindle-shaped cells in the fibrotic lesions of the pressure-overloaded left ventricles by immunohistochemistry. These cells were demonstrated by electron microscopy to have features specific for activated fibroblasts such as serrated nuclei or prominent rough endoplasmic reticulum. These cells also had characteristic features of myofibroblasts, i.e. irregularly arranged actin filaments and scattered dense bodies. Northern blot analysis revealed increased mRNA levels of SMemb both in aorta-constricted rat hearts and in cultured cardiac fibroblasts stimulated by TGF-β1 or by mechanical stretch. These results suggest that SMemb may be a molecular marker both for the detection of activated cardiac fibroblasts that may play important roles in the remodeling of pressure-overloaded cardiac interstitium, and for the identification of the regulatory mechanisms that control the phenotypic modulation of cardiac fibroblasts in response to pressure overload.
- Japanese Heart Journal Associationの論文
著者
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NAGAI Ryozo
Department of Cardiovascular Medicine, University of Tokyo
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Yazaki Yoshio
Department of Gene Diagnostics and Therapeutics, Research Institute, International Medical Center of
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Shiojima Ichiro
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine
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Shiojima Ichiro
千葉大学 医学研究院循環病態医科学
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Suzuki Jun-ichi
First Department Of Medicine Hokkaido University School Of Medicine
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Suzuki Jun-ichi
First Department Of Internal Medicine Shinshu University School Of Medicine
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AIKAWA Masanori
Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan
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Yazaki Yoshio
Department Of Cardiology University Of Tokyo
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Nagai Ryozo
Department Cardiovascular Medicine The University Of Tokyo Hospital
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SHIOJIMA Ichiro
Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Tokyo, Japan
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