Key result
CELF1 knockdown disrupts myofibrillar organization, suppresses cardiomyocyte proliferation, and impairs cardiac contraction.
Why the study?
The roles of CELF1 during cardiac development have not been completely elucidated.
CELF1 is essential for normal myofibril organization, proliferation, morphogenesis, and contractile performance in the developing embryonic myocardium.
CELF1 supports myofibrillar organization and proliferation in embryonic cardiomyocytes; leaves open conservation and relevance to human congenital heart disease.
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. Developmental Dynamics 245:854-873, 2016.
No takes yet. Share an insight, caveat, or question.
Blech‐Hermoni et al. (2016) studied Embryonic heart development. Knockdown of CELF1 was evaluated on Myofibrillar organization, proliferation, morphogenesis, and contractile function. Knockdown of CELF1 in embryonic models disrupted myofibrillar organization, reduced proliferation, and impaired cardiac contraction, demonstrating its requirement for normal myocardial development.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: