ArticleScientific reports2019
Versican is crucial for the initiation of cardiovascular lumen development in medaka (Oryzias latipes).
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Versican regulating viscoelasticity drives pleural fibrosis via mechanotransductive signaling.JCI insight · 2026Article
- Review
- morphoHeart: A quantitative tool for integrated 3D morphometric analyses of heart and ECM during embryonic development.PLoS biology · 2025Article
- Versican controlled by Lmx1b regulates hyaluronate density and hydration for semicircular canal morphogenesis.Development (Cambridge, England) · 2025Article
- Framing Heartaches: The Cardiac ECM and the Effects of Age.International journal of molecular sciences · 2023Review
- Article
- Polarized transport of membrane and secreted proteins during lumen morphogenesis.Seminars in cell & developmental biology · 2023Review
- Shutdown corner, a large deletion mutant isolated from a haploid mutagenesis screen in zebrafish.G3 (Bethesda, Md.) · 2022Article
- Neuron navigator 3 (NAV3) is required for heart development in zebrafish.Fish physiology and biochemistry · 2022Article
- Asymmetric Hapln1a drives regionalized cardiac ECM expansion and promotes heart morphogenesis in zebrafish development.Cardiovascular research · 2022Article
- Isolation and Purification of Versican and Analysis of Versican Proteolysis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Embryonic Onset of Sexually Dimorphic Heart Rates in the Viviparous Fish,Biomedicines · 2021Article
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Versican is an evolutionary conserved extracellular matrix proteoglycan, and versican expression loss in mice results in embryonic lethality owing to cardiovascular defects. However, the in utero development of mammals limits our understanding of the precise role of versican during cardiovascular development. Therefore, the use of evolutionarily distant species that develop ex utero is more suitable for studying the mechanistic basis of versican activity. We performed ENU mutagenesis screening to identify medaka mutants with defects in embryonic cardiovascular development. In this study, we described a recessive point mutation in the versican 3'UTR resulting in reduced versican protein expression. The fully penetrant homozygous mutant showed termination of cardiac development at the linear heart tube stage and exhibited absence of cardiac looping, a constricted outflow tract, and no cardiac jelly. Additionally, progenitor cells did not migrate from the secondary source towards the arterial pole of the linear heart tube, resulting in a constricted outflow tract. Furthermore, mutants lacked blood flow and vascular lumen despite continuous peristaltic heartbeats. These results enhance our understanding of the mechanistic basis of versican in cardiac development, and this mutant represents a novel genetic model to investigate the mechanisms of vascular tubulogenesis.
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