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Differential expression of α-enolase in the normal and pathological cardiac growth

It was found that α-enolase was dramatically up-regulated in the hypertrophic hearts of SHR in our previous study. The purposes of this study were to examine the expression pattern of α-enolase in pre- and postnatal myocardium of spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rats, and...

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Published in:Experimental and molecular pathology 2009-08, Vol.87 (1), p.27-31
Main Authors: Zhu, Li-an, Fang, Ning-yuan, Gao, Ping-jin, Jin, Xian, Wang, Hai-ya
Format: Article
Language:English
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Summary:It was found that α-enolase was dramatically up-regulated in the hypertrophic hearts of SHR in our previous study. The purposes of this study were to examine the expression pattern of α-enolase in pre- and postnatal myocardium of spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rats, and to explore the relationship between the overexpression of α-enolase and left ventricular hypertrophy. HE staining was used for the measurement of cardiac hypertrophy. Immunohistochemical technique was used to evaluate the location of α-enolase. The expressions of α-enolase in the left cardiac ventricles at different development times were examined by Real-time RT-PCR and Western blot. Cardiac hypertrophy was found in SHR rats at 4 weeks of age and remained up to 24 weeks of age. The signals of α-enolase protein were strong and existed extensively in hypertrophic myocardium in SHR, while in the normal myocardium of WKY, the signals were scarcely found and weak. The levels of α-enolase mRNA and protein in SHR and WKY hearts during fetal stage and newborn stage were similar, while from 4 weeks of age to 24 weeks of age, accompanied by the cardiac hypertrophy, the levels of α-enolase mRNA and protein in left ventricle of SHR were significantly higher than that in WKY. The expressions of α-enolase in the left ventricle of the rats during normal and pathological cardiac development were different. This phenomenon provides the potential clues to understanding pathophysiological mechanisms in cardiac hypertrophy of SHR.
ISSN:0014-4800
1096-0945
DOI:10.1016/j.yexmp.2009.05.002