ArticlePloS one2014
Imbalanced expression of Vcan mRNA splice form proteins alters heart morphology and cellular protein profiles.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Multimodal Evaluation and Management of Wagner Syndrome-Three Patients from an Affected Family.Genes · 2024Article
- Proteomics and bioinformatics analysis of cardiovascular related proteins in offspring exposed to gestational diabetes mellitus.Frontiers in cardiovascular medicine · 2022Article
- The versican-hyaluronan complex provides an essential extracellular matrix niche for Flk1Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Guide Cells Support Muscle Regeneration and Affect Neuro-Muscular Junction Organization.International journal of molecular sciences · 2021Article
- Muscularization of the Mesenchymal Outlet Septum during Cardiac Development.Journal of cardiovascular development and disease · 2020Review
- Versican: A Dynamic Regulator of the Extracellular Matrix.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Identification of key genes in atrial fibrillation using bioinformatics analysis.BMC cardiovascular disorders · 2020Article
- Genetic reduction of the extracellular matrix protein versican attenuates inflammatory cell infiltration and improves contractile function in dystrophic mdx diaphragm muscles.Scientific reports · 2020Article
- Profiling analysis of long non-coding RNAs in early postnatal mouse hearts.Scientific reports · 2017Article
- Probing chromatin landscape reveals roles of endocardial TBX20 in septation.The Journal of clinical investigation · 2016Article
- Characterization of the Transcriptional Complexity of the Receptive and Pre-receptive Endometria of Dairy Goats.Scientific reports · 2015Article
- Article
- Gene expression profiling by mRNA array reveals different pattern in Chinese glioblastoma patients between Uygur and Han populations.International journal of clinical and experimental medicine · 2015Article
- Differential expression and clinical significance of glioblastoma mRNA expression profiles in Uyghur and Han patients in Xinjiang province.Medical science monitor : international medical journal of experimental and clinical research · 2014Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The fundamental importance of the proteoglycan versican to early heart formation was clearly demonstrated by the Vcan null mouse called heart defect (hdf). Total absence of the Vcan gene halts heart development at a stage prior to the heart's pulmonary/aortic outlet segment growth. This creates a problem for determining the significance of versican's expression in the forming valve precursors and vascular wall of the pulmonary and aortic roots. This study presents data from a mouse model, Vcan ((tm1Zim)), of heart defects that results from deletion of exon 7 in the Vcan gene. Loss of exon 7 prevents expression of two of the four alternative splice forms of the Vcan gene. Mice homozygous for the exon 7 deletion survive into adulthood, however, the inability to express the V2 or V0 forms of versican results in ventricular septal defects, smaller cushions/valve leaflets with diminished myocardialization and altered pulmonary and aortic outflow tracts. We correlate these phenotypic findings with a large-scale differential protein expression profiling to identify compensatory alterations in cardiac protein expression at E13.5 post coitus that result from the absence of Vcan exon 7. The Vcan ((tm1Zim)) hearts show significant changes in the relative abundance of several cytoskeletal and muscle contraction proteins including some previously associated with heart disease. These alterations define a protein fingerprint that provides insight to the observed deficiencies in pre-valvular/septal cushion mesenchyme and the stability of the myocardial phenotype required for alignment of the outflow tract with the heart ventricles.
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