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首页> 外文期刊>Developmental dynamics: an official publication of the American Association of Anatomists >CUG-BP, Elav-like Family Member 1 (CELF1) is Required for Normal Myofibrillogenesis, Morphogenesis, and Contractile Function in the Embryonic Heart
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CUG-BP, Elav-like Family Member 1 (CELF1) is Required for Normal Myofibrillogenesis, Morphogenesis, and Contractile Function in the Embryonic Heart

机译：COUG-BP，胚胎心肌发生，形态发生和胚胎心脏的收缩功能所需

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Background: CUG-BP, Elav-like family member 1 (CELF1) is a multifunctional RNA binding protein found in a variety of adult and embryonic tissues. In the heart, CELF1 is found exclusively in the myocardium. However, the roles of CELF1 during cardiac development have not been completely elucidated. Results: Myofibrillar organization is disrupted and proliferation is reduced following knockdown of CELF1 in cultured chicken primary embryonic cardiomyocytes. In vivo knockdown of Celf1 in developing Xenopus laevis embryos resulted in myofibrillar disorganization and a trend toward reduced proliferation in heart muscle, indicating conserved roles for CELF1 orthologs in embryonic cardiomyocytes. Loss of Celf1 also resulted in morphogenetic abnormalities in the developing heart and gut. Using optical coherence tomography, we showed that cardiac contraction was impaired following depletion of Celf1, while heart rhythm remained unperturbed. In contrast to cardiac muscle, loss of Celf1 did not disrupt myofibril organization in skeletal muscle cells, although it did lead to fragmentation of skeletal muscle bundles. Conclusions: CELF1 is required for normal myofibril organization, proliferation, morphogenesis, and contractile performance in the developing myocardium. (C) 2016 Wiley Periodicals, Inc.
机译：背景：Cug-BP，蜂窝状家庭成员1（Celf1）是在各种成人和胚胎组织中发现的多功能RNA结合蛋白。在心脏中，Celf1仅在心肌中发现。然而，Celf1在心脏发育过程中的角色尚未完全阐明。结果：Myofibrillar组织被破坏，并且在培养的鸡初级胚胎心肌细胞中敲低Celf1敲低的增殖降低。在体内敲击Xenopus Laevis胚胎中的Celf 1敲低导致MyOfibrar紊乱和心肌增殖降低的趋势，表明Celf1直脑中的胚胎心肌细胞中的保守作用。 Celf1的丧失也导致了发展心脏和肠道的形态发生异常。使用光学相干断层扫描，我们表明Celf1耗尽后心脏收缩损害，而心律节奏仍然不受干扰。与心肌相比，Celf1的丧失不会破坏骨骼肌细胞中的肌纤维组织，尽管它确实导致骨骼肌束的破碎。结论：在培养的心肌中正常肌纤维组织，增殖，形态发生和收缩性能需要Celf1。 （c）2016 Wiley期刊，Inc。

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