ArticleProtein & cell2019
Dgcr8 deletion in the primitive heart uncovered novel microRNA regulating the balance of cardiac-vascular gene program.
Article in Protein & cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Cardiopulmonary progenitors facilitate cardiac repair via exosomal transfer of miR-27b-3p targeting the SIK1-CREB1 axis.Cell proliferation · 2024Article
- Dgcr8 functions in the secondary heart field for outflow tract and right ventricle development in mammals.Developmental biology · 2024Article
- RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024Article
- Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis.International journal of molecular sciences · 2022Review
- MicroRNA-151 Attenuates Apoptosis of Endothelial Cells Induced by Oxidized Low-density Lipoprotein by Targeting Interleukin-17A (IL-17A).Journal of cardiovascular translational research · 2021Article
- Control of ribosomal protein synthesis by the Microprocessor complex.Science signaling · 2021Article
- Review
- Genetic polymorphism in DGCR8 is associated with late onset of preeclampsia.BMC medical genetics · 2019Article
- Manganese dioxide nanosheets: from preparation to biomedical applications.International journal of nanomedicine · 2019Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window. We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mesp1 cardiovascular progenitor cells lead to the formation of extremely dilated and enlarged heart due to defective cardiomyocyte (CM) differentiation. Transcriptome analysis revealed unusual upregulation of vascular gene expression in Dgcr8 cKO hearts. Single cell RNA sequencing study further confirmed the increase of angiogenesis genes in single Dgcr8 cKO CM. We also performed global microRNA profiling of E9.5 heart for the first time, and identified that miR-541 was transiently highly expressed in E9.5 hearts. Interestingly, introducing miR-541 back into microRNA-free CMs partially rescued their defects, downregulated angiogenesis genes and significantly upregulated cardiac genes. Moreover, miR-541 can target Ctgf and inhibit endothelial function. Our results suggest that microRNAs are required to suppress abnormal angiogenesis gene program to maintain CM differentiation.
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Registered trials
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