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心肌中核CUG-BP、Elav样家族(CELF)活性受抑制的小鼠心肌病自发逆转过程中的基因表达分析

Gene Expression Analyses during Spontaneous Reversal of Cardiomyopathy in Mice with Repressed Nuclear CUG-BP, Elav-Like Family (CELF) Activity in Heart Muscle.

作者信息

Dasgupta Twishasri, Coram Ryan J, Stillwagon Samantha J, Ladd Andrea N

机构信息

Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America.

出版信息

PLoS One. 2015 Apr 20;10(4):e0124462. doi: 10.1371/journal.pone.0124462. eCollection 2015.

DOI:10.1371/journal.pone.0124462
PMID:25894229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4404138/
Abstract

CUG-BP, Elav-like family (CELF) proteins regulate cell type- and developmental stage-specific alternative splicing in the heart. Repression of CELF-mediated splicing activity via expression of a nuclear dominant negative CELF protein in heart muscle was previously shown to induce dysregulation of alternative splicing, cardiac dysfunction, cardiac hypertrophy, and dilated cardiomyopathy in MHC-CELFΔ transgenic mice. A "mild" line of MHC-CELFΔ mice that expresses a lower level of the dominant negative protein exhibits cardiac dysfunction and myopathy at a young age, but spontaneously recovers normal cardiac function and heart size with age despite the persistence of splicing defects. To the best of our knowledge, this was the first example of a genetically induced cardiomyopathy that spontaneously recovers without intervention. In this study, we explored the basis for this recovery. We examined whether a transcriptional program regulated by serum response factor (SRF) that is dysregulated in juvenile MHC-CELFΔ mice is restored in the mild line with age, and evaluated global changes in gene expression by microarray analyses. We found that differences in gene expression between the mild line and wild type hearts are greatly reduced in older animals, including a partial recovery of SRF target gene expression. We did not find evidence of a new compensatory pathway being activated in the mild line with age, and propose that recovery may occur due to developmental stage-specific compatibility of CELF-dependent splice variants with the cellular environment of the cardiomyocyte.

摘要

CUG-BP、Elav样家族(CELF)蛋白在心脏中调节细胞类型和发育阶段特异性的可变剪接。先前的研究表明,通过在心肌中表达核显性负性CELF蛋白来抑制CELF介导的剪接活性,会在MHC-CELFΔ转基因小鼠中诱导可变剪接失调、心脏功能障碍、心脏肥大和扩张型心肌病。表达较低水平显性负性蛋白的“轻度”MHC-CELFΔ小鼠品系在年轻时表现出心脏功能障碍和肌病,但尽管存在剪接缺陷,随着年龄增长仍能自发恢复正常心脏功能和心脏大小。据我们所知,这是首例未经干预即可自发恢复的基因诱导型心肌病。在本研究中,我们探究了这种恢复的基础。我们研究了在幼年MHC-CELFΔ小鼠中失调的由血清反应因子(SRF)调控 的转录程序在轻度品系中是否随年龄增长而恢复,并通过微阵列分析评估了基因表达的整体变化。我们发现,在老年动物中,轻度品系与野生型心脏之间的基因表达差异大幅减少,包括SRF靶基因表达的部分恢复。我们没有发现随着年龄增长轻度品系中有新的补偿途径被激活的证据,并提出恢复可能是由于CELF依赖性剪接变体与心肌细胞的细胞环境在发育阶段具有特异性相容性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/0b9978309c91/pone.0124462.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/36f8c72968d8/pone.0124462.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/690af06c7423/pone.0124462.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/300c12ff1146/pone.0124462.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/6fd52b2147f6/pone.0124462.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/0b9978309c91/pone.0124462.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/36f8c72968d8/pone.0124462.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/690af06c7423/pone.0124462.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/300c12ff1146/pone.0124462.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/6fd52b2147f6/pone.0124462.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14a3/4404138/0b9978309c91/pone.0124462.g005.jpg

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本文引用的文献

1
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2
Reactivation of fetal splicing programs in diabetic hearts is mediated by protein kinase C signaling.糖尿病心脏中胎儿剪接程序的再激活是由蛋白激酶 C 信号介导的。
J Biol Chem. 2013 Dec 6;288(49):35372-86. doi: 10.1074/jbc.M113.507426. Epub 2013 Oct 22.
3
Gene expression analyses implicate an alternative splicing program in regulating contractile gene expression and serum response factor activity in mice.
胚胎心肌中CUG结合蛋白、Elav样家族成员1(CELF1)调控靶点的鉴定
PLoS One. 2016 Feb 11;11(2):e0149061. doi: 10.1371/journal.pone.0149061. eCollection 2016.
基因表达分析表明,在小鼠中,一个可变剪接程序参与调节收缩基因表达和血清反应因子活性。
PLoS One. 2013;8(2):e56590. doi: 10.1371/journal.pone.0056590. Epub 2013 Feb 20.
4
'Ryanopathy': causes and manifestations of RyR2 dysfunction in heart failure.“Ryanopathy”:心力衰竭中 RyR2 功能障碍的原因和表现。
Cardiovasc Res. 2013 May 1;98(2):240-7. doi: 10.1093/cvr/cvt024. Epub 2013 Feb 12.
5
Cardiac ryanodine receptors control heart rate and rhythmicity in adult mice.心脏兰尼碱受体控制成年小鼠的心率和节律性。
Cardiovasc Res. 2012 Dec 1;96(3):372-80. doi: 10.1093/cvr/cvs260. Epub 2012 Aug 6.
6
Modulation of cardiac contractility by the phospholamban/SERCA2a regulatome.磷酸化兰尼碱受体/肌浆网钙 ATP 酶 2a 调节蛋白对心肌收缩力的调节。
Circ Res. 2012 Jun 8;110(12):1646-60. doi: 10.1161/CIRCRESAHA.111.259754.
7
Developmental expression and cardiac transcriptional regulation of Myh7b, a third myosin heavy chain in the vertebrate heart.脊椎动物心脏中第三种肌球蛋白重链 Myh7b 的发育表达和心脏转录调控。
Cytoskeleton (Hoboken). 2012 May;69(5):324-35. doi: 10.1002/cm.21029. Epub 2012 Apr 30.
8
The importance of CELF control: molecular and biological roles of the CUG-BP, Elav-like family of RNA-binding proteins.CELF 调控的重要性:CUG-BP、Elav 样 RNA 结合蛋白家族的分子和生物学作用。
Wiley Interdiscip Rev RNA. 2012 Jan-Feb;3(1):104-21. doi: 10.1002/wrna.107. Epub 2011 Aug 17.
9
The human phospholamban Arg14-deletion mutant localizes to plasma membrane and interacts with the Na/K-ATPase.人磷酸化酶抑素 Arg14 缺失突变体定位于质膜,并与 Na/K-ATP 酶相互作用。
J Mol Cell Cardiol. 2012 Mar;52(3):773-82. doi: 10.1016/j.yjmcc.2011.11.012. Epub 2011 Dec 1.
10
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Hypertension. 2011 Dec;58(6):1099-110. doi: 10.1161/HYPERTENSIONAHA.111.173500. Epub 2011 Oct 10.