ArticleScientific reports2017
Regulation of Sema3c and the Interaction between Cardiac Neural Crest and Second Heart Field during Outflow Tract Development.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 64 citations in OpenAlex.
- A noncanonical role for Jagged1 in endothelial mechanotransduction.The FEBS journal · 2026Article
- An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Environmentally dependent developmental induction as a potential driver of heart evolution.The Journal of experimental biology · 2026Review
- Fibroblast growth factor 8: Multifaceted role in development and developmental disorder.Genes & diseases · 2025Review
- De novo variant in RING finger protein 213 causes systemic vasculopathy.JCI insight · 2025Article
- Morphological Alterations of Conal Ridges and Differential Expression of AP2α in the Offspring Hearts of Experimental Diabetic Rats.International journal of molecular sciences · 2025Article
- Origins of Aortic Coarctation: A Vascular Smooth Muscle Compartment Boundary Model.Journal of developmental biology · 2025Article
- The chromatin regulator Ankrd11 controls cardiac neural crest cell-mediated outflow tract remodeling and heart function.Nature communications · 2024Article
- In-Depth Genomic Analysis: The New Challenge in Congenital Heart Disease.International journal of molecular sciences · 2024Review
- Novel pathogenic GATA6 variant associated with congenital heart disease, diabetes mellitus and necrotizing enterocolitis.Pediatric research · 2024Article
- Human Genetics of Truncus Arteriosus.Advances in experimental medicine and biology · 2024Review
- Polarity and migration of cranial and cardiac neural crest cells: underlying molecular mechanisms and disease implications.Frontiers in cell and developmental biology · 2024Review
- An Anterior Second Heart Field Enhancer Regulates the Gene Regulatory Network of the Cardiac Outflow Tract.Circulation · 2023Article
- Analysis of theTranslational pediatrics · 2023Article
- Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development.Nature communications · 2023Article
- Variations in the poly-histidine repeat motif of HOXA1 contribute to bicuspid aortic valve in mouse and zebrafish.Nature communications · 2023Article
- A phenotypic rescue approach identifies lineage regionalization defects in a mouse model of DiGeorge syndrome.Disease models & mechanisms · 2022Article
- Clinical Developmental Cardiology for Understanding Etiology of Congenital Heart Disease.Journal of clinical medicine · 2022Review
- Genomic frontiers in congenital heart disease.Nature reviews. Cardiology · 2022Review
- Modeling Paracrine Noncanonical Wnt Signaling In Vitro.Journal of visualized experiments : JoVE · 2021Article
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cardiac neural crest cells (cNCCs) and the second heart field (SHF) play key roles in development of the cardiac outflow tract (OFT) for establishment of completely separated pulmonary and systemic circulations in vertebrates. A neurovascular guiding factor, Semaphorin 3c (Sema3c), is required for the development of the OFT, however, its regulation of the interaction between cNCCs and SHF remains to be determined. Here, we show that a Sema3c is a candidate that mediates interaction between cNCCs and the SHF during development of the OFT. Foxc1/c2 directly activates the transcription of Sema3c in the OFT, whereas, a hypomorph of Tbx1, a key SHF transcription factor, resulted in the ectopic expression of Sema3c in the pharyngeal arch region. Fgf8, a downstream secreted factor of Tbx1, inhibited the expression of Sema3c in cNCCs via activation of ERK1/2 signaling. Blocking of FGF8 caused ectopic expression of SEMA3C and a migration defect of cNCCs, resulting in abnormal chick pharyngeal arch development. These results suggest that proper spatio-temporal expression of Sema3c, regulated positively by Foxc1/c2 and negatively by the Tbx1-Fgf8 cascade, respectively, is essential for the interaction between cNCCs and the SHF that correctly navigates cNCCs towards the OFT, composed of SHF-derived cells.
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