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Inherited cardiomyopathies caused by troponin mutations

Journal of Geriatric Cardiology 2013年第1期10卷 91-101页

作者： Qun-Wei Lu Xiao-Yan Wu Sachio Morimoto Key Laboratory of Molecular Biophysics of Ministry of Education College of Life Science and Technology Center for Human Genome Research Huazhong University of Science and Technology Wuhan 430074 China Department of Pediatrics Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Department of Clinical Pharmacology Graduate School of Medical Sciences Kyushu University Fukuoka 812-8582 Japan

Genetic investigations of cardiomyopathy in the recent two decades have revealed a large number of mutations in the genes encoding sarcomeric proteins as a cause of inherited hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), or restrictive cardiomyopathy (RCM). Most functional analyses of the effects of mutations on cardiac muscle contraction have revealed significant changes in the Ca2+-regulatory mechanism, in which cardiac troponin (cTn) plays important structural and functional roles as a key regulatory protein. Over a hundred mutations have been identified in all three subunits of cTn, i.e., cardiac troponins T, I, and C. Recent studies on cTn mutations have provided plenty of evidence that HCM- and RCM-linked mutations increase cardiac myofilament Ca2+ sensitivity, while DCM-linked mutations decrease it. This review focuses on the functional consequences of mutations found in cTn in terms of cardiac myofilament Ca2+ sensitivity, ATPase activity, force generation, and cardiac troponin I phosphorylation, to understand potential molecular and cellular pathogenic mechanisms of the three types of inherited cardiomyopathy.

关键词： calcium sensitivity Cardiomyopathy Muscle contraction Troponin

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The pharmacological characterization of martentoxin on glioma BK channels

The pharmacological characterization of martentoxin on gliom...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Ying CHEN,Jian SHI,Yan-Hong DUAN,Lei ZHONG,Yong-Hua JI School of Life Sciences,Shanghai University,Shanghai 200444,China

Martentoxin as a 37 residues peptide purified from the venom of Chinese scorpion Buthus martensi Karch(BmK) was capable of blocking large-conductance Ca-activated K(BK) channels in adrenal medulla chromaffin cells with a great *** the present study,the pharmacological effect of martentoxin on glioma BK channels(gBK),which was a splice variant of hsloαsubunits,was investigated through the electrophysiological *** results revealed that gBK were blocked by martentoxin in the absence of cytosolic Ca The inhibitory effect of martentoxin on gBK was conversed to an enhancive effect in the presence of cytosolic *** enhancement occurred without voltage-dependence but ***,martentoxin could decrease the inhibitory effect of iberiotoxin or tetrabutylammonium chloride on gBK with free Ca in the *** imaging showed that martentoxin could not evoke the oscillation of cytoplasmic Ca concentration and excluded the possible influence of martentoxin on cytosolic Ca. Therefore,the results suggested that the pharmacological effect of martentoxin on gBK was decided by cytosolic Ca and the interaction site of gBK for martentoxin might be different from that for Ibtx or tetrabutylammonium *** present study shed light on a novel mode for the interaction between neurotoxins and K channels and may provide a potential design for the BK channel-specific tool.

关键词： BK channel glioma martentoxin calcium sensitivity iberiotoxin

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