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High salt-induced excess reactive oxygen species production resulted in heart tube malformation during gastrulation
- An association has been proved between high salt consumption and cardiovascular mortality. In vertebrates, the heart is the first functional organ to be formed. However, it is not clear whether high-salt exposure has an adverse impact on cardiogenesis. Here we report high-salt exposure inhibited basement membrane breakdown by affecting RhoA, thus disturbing the expression of Slug/E-cadherin/N-cadherin/Laminin and interfering with mesoderm formation during the epithelial-mesenchymal transition(EMT). Furthermore, the DiI(+) cell migration trajectory in vivo and scratch wound assays in vitro indicated that high-salt exposure restricted cell migration of cardiac progenitors, which was caused by the weaker cytoskeleton structure and unaltered corresponding adhesion junctions at HH7. Besides, down-regulation of GATA4/5/6, Nkx2.5, TBX5, and Mef2c and up-regulation of Wnt3a/-catenin caused aberrant cardiomyocyte differentiation at HH7 and HH10. High-salt exposure also inhibited cell proliferation and promoted apoptosis. Most importantly, ourAn association has been proved between high salt consumption and cardiovascular mortality. In vertebrates, the heart is the first functional organ to be formed. However, it is not clear whether high-salt exposure has an adverse impact on cardiogenesis. Here we report high-salt exposure inhibited basement membrane breakdown by affecting RhoA, thus disturbing the expression of Slug/E-cadherin/N-cadherin/Laminin and interfering with mesoderm formation during the epithelial-mesenchymal transition(EMT). Furthermore, the DiI(+) cell migration trajectory in vivo and scratch wound assays in vitro indicated that high-salt exposure restricted cell migration of cardiac progenitors, which was caused by the weaker cytoskeleton structure and unaltered corresponding adhesion junctions at HH7. Besides, down-regulation of GATA4/5/6, Nkx2.5, TBX5, and Mef2c and up-regulation of Wnt3a/-catenin caused aberrant cardiomyocyte differentiation at HH7 and HH10. High-salt exposure also inhibited cell proliferation and promoted apoptosis. Most importantly, our study revealed that excessive reactive oxygen species(ROS)generated by high salt disturbed the expression of cardiac-related genes, detrimentally affecting the above process including EMT, cell migration, differentiation, cell proliferation and apoptosis, which is the major cause of malformation of heart tubes.…
Author details: | Lin-rui Gao, Guang Wang, Jing Zhang, Shuai Li, Manli Chuai, Yongping Bao, Berthold HocherORCiDGND, Xuesong YangORCiD |
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DOI: | https://doi.org/10.1002/jcp.26528 |
ISSN: | 0021-9541 |
ISSN: | 1097-4652 |
Pubmed ID: | https://pubmed.ncbi.nlm.nih.gov/29574800 |
Title of parent work (English): | Journal of Cellular Physiology |
Publisher: | Wiley |
Place of publishing: | Hoboken |
Publication type: | Article |
Language: | English |
Date of first publication: | 2018/03/25 |
Publication year: | 2018 |
Release date: | 2021/10/11 |
Tag: | cardiac progenitor migration and differentiation; chick embryo; heart tube; high salt; reactive oxygen species |
Volume: | 233 |
Issue: | 9 |
Number of pages: | 14 |
First page: | 7120 |
Last Page: | 7133 |
Funding institution: | NSFCNational Natural Science Foundation of China [81741016, 31771331]; Science and Technology Planning Project of Guangdong Province [2017A020214015, 2017A050506029]; Science and Technology Program of Guangzhou [201710010054]; Guangdong Natural Science FoundationNational Natural Science Foundation of Guangdong Province [2016A030311044]; Fundamental Research Funds for the Central UniversitiesFundamental Research Funds for the Central Universities [21617466]; Students Research Training Program Fund [201610559024] |
Organizational units: | Mathematisch-Naturwissenschaftliche Fakultät / Institut für Ernährungswissenschaft |
DDC classification: | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Peer review: | Referiert |
Publishing method: | Open Access / Green Open-Access |