TY  - JOUR
A1  - Wang, Guang
A1  - Li, Pei-zhi
A1  - Zhang, Shi-yao
A1  - Zhong, Shan
A1  - Chu, Chang
A1  - Zeng, Shufei
A1  - Yan, Yu
A1  - Cheng, Xin
A1  - Chuai, Manli
A1  - Hocher, Berthold
A1  - Yang, Xuesong
T1  - Lipopolysaccharides (LPS) Induced Angiogenesis During Chicken Embryogenesis is Abolished by Combined ETA/ETB Receptor Blockade
JF  - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry and pharmacology
N2  - Background/Aims: Angiogenesis plays a key role during embryonic development. The vascular endothelin (ET) system is involved in the regulation of angiogenesis. Lipopolysaccharides (LPS) could induce angiogenesis. The effects of ET blockers on baseline and LPS-stimulated angiogenesis during embryonic development remain unknown so far. Methods: The blood vessel density (BVD) of chorioallantoic membranes (CAMs), which were treated with saline (control), LPS, and/or BQ123 and the ETB blocker BQ788, were quantified and analyzed using an IPP 6.0 image analysis program. Moreover, the expressions of ET-1, ET-2, ET3, ET receptor A (ETRA), ET receptor B (ETRB) and VEGFR2 mRNA during embryogenesis were analyzed by semi-quantitative RT-PCR. Results: All components of the ET system are detectable during chicken embryogenesis. LPS increased angiogenesis substantially. This process was completely blocked by the treatment of a combination of the ETA receptor blockers-BQ123 and the ETB receptor blocker BQ788. This effect was accompanied by a decrease in ETRA, ETRB, and VEGFR2 gene expression. However, the baseline angiogenesis was not affected by combined ETA/ETB receptor blockade. Conclusion: During chicken embryogenesis, the LPS-stimulated angiogenesis, but not baseline angiogenesis, is sensitive to combined ETA/ETB receptor blockade.
KW  - Lipopolysaccharides (LPS)
KW  - Angiogenesis
KW  - Chicken chorioallantoic membrane (CAM)
KW  - Endothelin (ET)
Y1  - 2018
U6  - https://doi.org/10.1159/000492547
SN  - 1015-8987
SN  - 1421-9778
VL  - 48
IS  - 5
SP  - 2084
EP  - 2090
PB  - Karger
CY  - Basel
ER  - 
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  -