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使用靶向核酸酶和联合疗法纠正与心肌病相关的人类磷酸受纳蛋白R14del突变。

Correction of human phospholamban R14del mutation associated with cardiomyopathy using targeted nucleases and combination therapy.

作者信息

Karakikes Ioannis, Stillitano Francesca, Nonnenmacher Mathieu, Tzimas Christos, Sanoudou Despina, Termglinchan Vittavat, Kong Chi-Wing, Rushing Stephanie, Hansen Jens, Ceholski Delaine, Kolokathis Fotis, Kremastinos Dimitrios, Katoulis Alexandros, Ren Lihuan, Cohen Ninette, Gho Johannes M I H, Tsiapras Dimitrios, Vink Aryan, Wu Joseph C, Asselbergs Folkert W, Li Ronald A, Hulot Jean-Sebastien, Kranias Evangelia G, Hajjar Roger J

机构信息

Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.

Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.

出版信息

Nat Commun. 2015 Apr 29;6:6955. doi: 10.1038/ncomms7955.

Abstract

A number of genetic mutations is associated with cardiomyopathies. A mutation in the coding region of the phospholamban (PLN) gene (R14del) is identified in families with hereditary heart failure. Heterozygous patients exhibit left ventricular dilation and ventricular arrhythmias. Here we generate induced pluripotent stem cells (iPSCs) from a patient harbouring the PLN R14del mutation and differentiate them into cardiomyocytes (iPSC-CMs). We find that the PLN R14del mutation induces Ca(2+) handling abnormalities, electrical instability, abnormal cytoplasmic distribution of PLN protein and increases expression of molecular markers of cardiac hypertrophy in iPSC-CMs. Gene correction using transcription activator-like effector nucleases (TALENs) ameliorates the R14del-associated disease phenotypes in iPSC-CMs. In addition, we show that knocking down the endogenous PLN and simultaneously expressing a codon-optimized PLN gene reverses the disease phenotype in vitro. Our findings offer novel strategies for targeting the pathogenic mutations associated with cardiomyopathies.

摘要

许多基因突变与心肌病相关。在遗传性心力衰竭家族中发现了磷酸受磷蛋白(PLN)基因编码区的一种突变(R14del)。杂合子患者表现出左心室扩张和室性心律失常。在此,我们从携带PLN R14del突变的患者中生成诱导多能干细胞(iPSC),并将其分化为心肌细胞(iPSC-CM)。我们发现PLN R14del突变在iPSC-CM中诱导钙(Ca2+)处理异常、电不稳定、PLN蛋白的异常细胞质分布,并增加心脏肥大分子标志物的表达。使用转录激活样效应核酸酶(TALEN)进行基因校正可改善iPSC-CM中与R14del相关的疾病表型。此外,我们表明敲低内源性PLN并同时表达密码子优化的PLN基因可在体外逆转疾病表型。我们的研究结果为针对与心肌病相关的致病突变提供了新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/352d/4421839/a83e07265345/ncomms7955-f1.jpg

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