TY  - JOUR
A1  - Gao, Lin-rui
A1  - Wang, Guang
A1  - Zhang, Jing
A1  - Li, Shuai
A1  - Chuai, Manli
A1  - Bao, Yongping
A1  - Hocher, Berthold
A1  - Yang, Xuesong
T1  - High salt-induced excess reactive oxygen species production resulted in heart tube malformation during gastrulation
JF  - Journal of Cellular Physiology
N2  - 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.
KW  - cardiac progenitor migration and differentiation
KW  - chick embryo
KW  - heart tube
KW  - high salt
KW  - reactive oxygen species
Y1  - 2018
U6  - https://doi.org/10.1002/jcp.26528
SN  - 0021-9541
SN  - 1097-4652
VL  - 233
IS  - 9
SP  - 7120
EP  - 7133
PB  - Wiley
CY  - Hoboken
ER  -