@article{GaoWangZhangetal.2018,
  author    = {Gao, Lin-rui and Wang, Guang and Zhang, Jing and Li, Shuai and Chuai, Manli and Bao, Yongping and Hocher, Berthold and Yang, Xuesong},
  title     = {High salt-induced excess reactive oxygen species production resulted in heart tube malformation during gastrulation},
  series = {Journal of Cellular Physiology},
  volume    = {233},
  journal   = {Journal of Cellular Physiology},
  number    = {9},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0021-9541},
  doi       = {10.1002/jcp.26528},
  pages     = {7120 -- 7133},
  year      = {2018},
  abstract  = {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, 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.},
  language  = {en}
}