The impact of high-salt exposure on cardiovascular development in the early chick embryo

Guang Wang, Nuan Zhang, Yi-Fan Wei, Yi-Mei Jin, Shi-Yao Zhang, Xin Cheng, Zheng-Lai Ma, Shu-Zhu Zhao, You-Peng Chen, Manli Chuai, Berthold Hocher (Lead / Corresponding author), Xuesong Yang (Lead / Corresponding author)

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-salt-suppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-salt-induced defects in heart and angiogenesis.

Original languageEnglish
Pages (from-to)3468-3477
Number of pages10
JournalJournal of Experimental Biology
Volume218
Issue number21
DOIs
Publication statusPublished - 4 Nov 2015

Fingerprint

Chick Embryo
early development
embryo
embryo (animal)
Salts
chicks
salt
salts
angiogenesis
Yolk Sac
heart
yolk sac
membrane
blood
apoptosis
Membranes
defect
reactive oxygen species
Reactive Oxygen Species
cell proliferation

Keywords

  • Animals
  • Antioxidants
  • Apoptosis
  • Cardiovascular abnormalities
  • Cell proliferation
  • Chick Embryo
  • Chorioallantoic membrane
  • Embryonic development
  • Gene expression regulation, Developmental
  • Heart
  • Human umbilical vein endothelial cells
  • Humans
  • Morphogenesis
  • Myocytes, Cardiac
  • Reactive oxygen species
  • Sodium Chloride
  • Yolk sac
  • Journal article
  • Research support, Non-U.S. Gov't

Cite this

Wang, G., Zhang, N., Wei, Y-F., Jin, Y-M., Zhang, S-Y., Cheng, X., ... Yang, X. (2015). The impact of high-salt exposure on cardiovascular development in the early chick embryo. Journal of Experimental Biology, 218(21), 3468-3477. https://doi.org/10.1242/jeb.129486
Wang, Guang ; Zhang, Nuan ; Wei, Yi-Fan ; Jin, Yi-Mei ; Zhang, Shi-Yao ; Cheng, Xin ; Ma, Zheng-Lai ; Zhao, Shu-Zhu ; Chen, You-Peng ; Chuai, Manli ; Hocher, Berthold ; Yang, Xuesong. / The impact of high-salt exposure on cardiovascular development in the early chick embryo. In: Journal of Experimental Biology. 2015 ; Vol. 218, No. 21. pp. 3468-3477.
@article{d0e2bcf12b8a40f69f449e0630cfdc44,
title = "The impact of high-salt exposure on cardiovascular development in the early chick embryo",
abstract = "In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-salt-suppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-salt-induced defects in heart and angiogenesis.",
keywords = "Animals, Antioxidants, Apoptosis, Cardiovascular abnormalities, Cell proliferation, Chick Embryo, Chorioallantoic membrane, Embryonic development, Gene expression regulation, Developmental, Heart, Human umbilical vein endothelial cells, Humans, Morphogenesis, Myocytes, Cardiac, Reactive oxygen species, Sodium Chloride, Yolk sac, Journal article, Research support, Non-U.S. Gov't",
author = "Guang Wang and Nuan Zhang and Yi-Fan Wei and Yi-Mei Jin and Shi-Yao Zhang and Xin Cheng and Zheng-Lai Ma and Shu-Zhu Zhao and You-Peng Chen and Manli Chuai and Berthold Hocher and Xuesong Yang",
note = "This study was supported by NSFC grant (81571436; 31401230); Medical Scientific Research Foundation of Guangdong Province (A2015201); Science and Technology Program of Guangzhou (201510010073); China Postdoctoral Science Foundation (2015T80940; 2014M560694); the Fundamental Research Funds for the Central Universities (21614319, 21615421); The Funds for Young Creative Talents of Higher Education in Guangdong Province (2014KQNCX026) and Students Research Training Program Fund (201410559032, 1210559035, CX13181).",
year = "2015",
month = "11",
day = "4",
doi = "10.1242/jeb.129486",
language = "English",
volume = "218",
pages = "3468--3477",
journal = "Journal of Experimental Biology",
issn = "0022-0949",
publisher = "Company of Biologists",
number = "21",

}

Wang, G, Zhang, N, Wei, Y-F, Jin, Y-M, Zhang, S-Y, Cheng, X, Ma, Z-L, Zhao, S-Z, Chen, Y-P, Chuai, M, Hocher, B & Yang, X 2015, 'The impact of high-salt exposure on cardiovascular development in the early chick embryo', Journal of Experimental Biology, vol. 218, no. 21, pp. 3468-3477. https://doi.org/10.1242/jeb.129486

The impact of high-salt exposure on cardiovascular development in the early chick embryo. / Wang, Guang; Zhang, Nuan; Wei, Yi-Fan; Jin, Yi-Mei; Zhang, Shi-Yao; Cheng, Xin; Ma, Zheng-Lai; Zhao, Shu-Zhu; Chen, You-Peng; Chuai, Manli; Hocher, Berthold (Lead / Corresponding author); Yang, Xuesong (Lead / Corresponding author).

In: Journal of Experimental Biology, Vol. 218, No. 21, 04.11.2015, p. 3468-3477.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The impact of high-salt exposure on cardiovascular development in the early chick embryo

AU - Wang, Guang

AU - Zhang, Nuan

AU - Wei, Yi-Fan

AU - Jin, Yi-Mei

AU - Zhang, Shi-Yao

AU - Cheng, Xin

AU - Ma, Zheng-Lai

AU - Zhao, Shu-Zhu

AU - Chen, You-Peng

AU - Chuai, Manli

AU - Hocher, Berthold

AU - Yang, Xuesong

N1 - This study was supported by NSFC grant (81571436; 31401230); Medical Scientific Research Foundation of Guangdong Province (A2015201); Science and Technology Program of Guangzhou (201510010073); China Postdoctoral Science Foundation (2015T80940; 2014M560694); the Fundamental Research Funds for the Central Universities (21614319, 21615421); The Funds for Young Creative Talents of Higher Education in Guangdong Province (2014KQNCX026) and Students Research Training Program Fund (201410559032, 1210559035, CX13181).

PY - 2015/11/4

Y1 - 2015/11/4

N2 - In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-salt-suppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-salt-induced defects in heart and angiogenesis.

AB - In this study, we show that high-salt exposure dramatically increases chick mortality during embryo development. As embryonic mortality at early stages mainly results from defects in cardiovascular development, we focused on heart formation and angiogenesis. We found that high-salt exposure enhanced the risk of abnormal heart tube looping and blood congestion in the heart chamber. In the presence of high salt, both ventricular cell proliferation and apoptosis increased. The high osmolarity induced by high salt in the ventricular cardiomyocytes resulted in incomplete differentiation, which might be due to reduced expression of Nkx2.5 and GATA4. Blood vessel density and diameter were suppressed by exposure to high salt in both the yolk sac membrane (YSM) and chorioallantoic membrane models. In addition, high-salt-induced suppression of angiogenesis occurred even at the vasculogenesis stage, as blood island formation was also inhibited by high-salt exposure. At the same time, cell proliferation was repressed and cell apoptosis was enhanced by high-salt exposure in YSM tissue. Moreover, the reduction in expression of HIF2 and FGF2 genes might cause high-salt-suppressed angiogenesis. Interestingly, we show that high-salt exposure causes excess generation of reactive oxygen species (ROS) in the heart and YSM tissues, which could be partially rescued through the addition of antioxidants. In total, our study suggests that excess generation of ROS might play an important role in high-salt-induced defects in heart and angiogenesis.

KW - Animals

KW - Antioxidants

KW - Apoptosis

KW - Cardiovascular abnormalities

KW - Cell proliferation

KW - Chick Embryo

KW - Chorioallantoic membrane

KW - Embryonic development

KW - Gene expression regulation, Developmental

KW - Heart

KW - Human umbilical vein endothelial cells

KW - Humans

KW - Morphogenesis

KW - Myocytes, Cardiac

KW - Reactive oxygen species

KW - Sodium Chloride

KW - Yolk sac

KW - Journal article

KW - Research support, Non-U.S. Gov't

U2 - 10.1242/jeb.129486

DO - 10.1242/jeb.129486

M3 - Article

VL - 218

SP - 3468

EP - 3477

JO - Journal of Experimental Biology

JF - Journal of Experimental Biology

SN - 0022-0949

IS - 21

ER -