ArticleInternational journal of molecular medicine2015
GATA4 transgenic mice as an in vivo model of congenital heart disease.
Article in International journal of molecular medicine, 2015. 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, 20 citations in OpenAlex.
- Cardiac Development and Factors Influencing the Development of Congenital Heart Defects (CHDs): Part I.International journal of molecular sciences · 2024Review
- DIO3 protects against thyrotoxicosis-derived cranio-encephalic and cardiac congenital abnormalities.JCI insight · 2022Article
- Towards Understanding the Gene-Specific Roles of GATA Factors in Heart Development: Does GATA4 Lead the Way?International journal of molecular sciences · 2022Review
- Alternative strategies in cardiac preclinical research and new clinical trial formats.Cardiovascular research · 2022Review
- The M310T mutation in the GATA4 gene is a novel pathogenic target of the familial atrial septal defect.BMC cardiovascular disorders · 2021Article
- Decoding Genetics of Congenital Heart Disease Using Patient-Derived Induced Pluripotent Stem Cells (iPSCs).Frontiers in cell and developmental biology · 2021Review
- Connection of GLI1 variants to congenital heart disease susceptibility: A case-control study.Medicine · 2020Observational
- Experimental Rodent Models of Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2020Review
- Genetic Basis for Congenital Heart Disease: Revisited: A Scientific Statement From the American Heart Association.Circulation · 2018Review
- [Establishment and verification of a mouse model ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- TBX1 loss-of-function mutation contributes to congenital conotruncal defects.Experimental and therapeutic medicine · 2018Article
- Utilization of Whole Exome Sequencing to Identify Causative Mutations in Familial Congenital Heart Disease.Circulation. Cardiovascular genetics · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study indicated that 8 patients from a family with a history of congenital heart disease had simple atrial septal defect (ASD) and carried the same mutation at codon 310 in the GATA4 gene. In the present study, to identify the functional defects caused by this mutation in an in vivo model, the transgene DNA constructs were microinjected into mice to generate a transgenic mouse model. The mice were genotyped using PCR and DNA sequencing. Protein expression was measured by western blot analysis. qPCR was used to determine the copy number of the transgenes. The heart tissue was fixed and sectioned by conventional procedures. The Vevo 2000 system was used to perform echocardiography on the mice. The expression of GATA4 target genes was measured using the real-time PCR system. The incidence of ASD in the heterozygous transgenic mice was found to be greater than that in the wild-type control mice (P<0.05). In addition, the expression of α-myosin heavy chain (α-MHC) in the heart tissues from the homozygous mice was lower than that in the heart tissues from their wild-type littermates (P<0.05). In conclusion, these results suggest that the introduction of GATA4 M310V negatively affects the normal expression of α-MHC. In accordance with previous findings on GATA4 mutation screening and in vitro experiments, this study confirms that GATA4 M310V mutation may lead to the development of the congenital heart defect, ASD.
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