Gut microbiota-derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis

Jing Zhang, Guang Wang, Jia Liu, Lin-rui Gao, Meng Liu, Chao-Jie Wang, Manli Chuai, Yongping Bao, Ge Li, Rui-Man Li, Yu Zhang, Xuesong Yang (Lead / Corresponding author)

Research output: Contribution to journalArticle

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Abstract

Background: Cytotoxicity and inflammation-associated toxic responses could be induced by bacterial lipopolysaccharides (LPS) in vitro and in vivo respectively. However, the mechanism involved in LPS-induced cardiac malformation in prenatal fetus is still unknown.

Methods and results: In this study, we demonstrated that LPS was induced in gut microbiota imbalance mice, and next, LPS exposure during gastrulation in the chick embryo increased the incidence of cardia bifida. Gene transfection and tissue transplantation trajectory indicated that LPS exposure restricted the cell migration of cardiac progenitors to primary heart field in gastrula chick embryos. In vitro explant allograft of GFP-labeled anterior primitive streak demonstrated that LPS treatments could inhibit cell migration. A similar observation was also obtained from the cell migration assay of scratch wounds using primary culture of cardiomyocytes or H9c2 cells. In the embryos exposed to LPS, expressions of Nkx2.5 and GATA5 were disturbed. These genes are associated with cardiomyocyte differentiation when heart tube fusion occurs. Furthermore, pHIS3, C-caspase3 immunohistological staining indicated that cell proliferation decreased, cell apoptosis increased in the heart tube of chick embryo. Meanwhile, in vivo, pHIS3 immunohistological staining and Hochest/PI staining also draw the similar conclusions. The LPS exposure also caused the production of excess ROS, which might damage the cardiac precursor cells of developing embryos. At last, we showed that LPS-induced cardia bifida could be partially rescued through the addition of antioxidants.

Conclusions: Together, these results reveal that excess ROS generation is involved in the LPS-induced defects in heart tube during chick embryo development. This article is protected by copyright. All rights reserved.

Original languageEnglish
Pages (from-to)9271-9283
Number of pages13
JournalJournal of Cellular Physiology
Volume233
Issue number12
Early online date8 Sep 2017
DOIs
Publication statusPublished - Dec 2018

Fingerprint

Cardia
Endotoxins
Lipopolysaccharides
Incidence
Chick Embryo
Staining and Labeling
Cardiac Myocytes
Cell Movement
Embryonic Structures
Genes
Cell Migration Assays
Primitive Streak
Gastrointestinal Microbiome
Transplantation (surgical)
Gastrula
Tissue Transplantation
Gastrulation
Poisons
Cell proliferation
Cytotoxicity

Keywords

  • Lipopolysaccharides
  • Chick Embryo
  • Reactive oxygen species
  • Heart Tube

Cite this

Zhang, J., Wang, G., Liu, J., Gao, L., Liu, M., Wang, C-J., ... Yang, X. (2018). Gut microbiota-derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis. Journal of Cellular Physiology, 233(12), 9271-9283. https://doi.org/10.1002/jcp.26175
Zhang, Jing ; Wang, Guang ; Liu, Jia ; Gao, Lin-rui ; Liu, Meng ; Wang, Chao-Jie ; Chuai, Manli ; Bao, Yongping ; Li, Ge ; Li, Rui-Man ; Zhang, Yu ; Yang, Xuesong. / Gut microbiota-derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis. In: Journal of Cellular Physiology. 2018 ; Vol. 233, No. 12. pp. 9271-9283.
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abstract = "Background: Cytotoxicity and inflammation-associated toxic responses could be induced by bacterial lipopolysaccharides (LPS) in vitro and in vivo respectively. However, the mechanism involved in LPS-induced cardiac malformation in prenatal fetus is still unknown.Methods and results: In this study, we demonstrated that LPS was induced in gut microbiota imbalance mice, and next, LPS exposure during gastrulation in the chick embryo increased the incidence of cardia bifida. Gene transfection and tissue transplantation trajectory indicated that LPS exposure restricted the cell migration of cardiac progenitors to primary heart field in gastrula chick embryos. In vitro explant allograft of GFP-labeled anterior primitive streak demonstrated that LPS treatments could inhibit cell migration. A similar observation was also obtained from the cell migration assay of scratch wounds using primary culture of cardiomyocytes or H9c2 cells. In the embryos exposed to LPS, expressions of Nkx2.5 and GATA5 were disturbed. These genes are associated with cardiomyocyte differentiation when heart tube fusion occurs. Furthermore, pHIS3, C-caspase3 immunohistological staining indicated that cell proliferation decreased, cell apoptosis increased in the heart tube of chick embryo. Meanwhile, in vivo, pHIS3 immunohistological staining and Hochest/PI staining also draw the similar conclusions. The LPS exposure also caused the production of excess ROS, which might damage the cardiac precursor cells of developing embryos. At last, we showed that LPS-induced cardia bifida could be partially rescued through the addition of antioxidants.Conclusions: Together, these results reveal that excess ROS generation is involved in the LPS-induced defects in heart tube during chick embryo development. This article is protected by copyright. All rights reserved.",
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Zhang, J, Wang, G, Liu, J, Gao, L, Liu, M, Wang, C-J, Chuai, M, Bao, Y, Li, G, Li, R-M, Zhang, Y & Yang, X 2018, 'Gut microbiota-derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis', Journal of Cellular Physiology, vol. 233, no. 12, pp. 9271-9283. https://doi.org/10.1002/jcp.26175

Gut microbiota-derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis. / Zhang, Jing; Wang, Guang; Liu, Jia; Gao, Lin-rui; Liu, Meng; Wang, Chao-Jie; Chuai, Manli; Bao, Yongping; Li, Ge; Li, Rui-Man; Zhang, Yu; Yang, Xuesong (Lead / Corresponding author).

In: Journal of Cellular Physiology, Vol. 233, No. 12, 12.2018, p. 9271-9283.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Gut microbiota-derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis

AU - Zhang, Jing

AU - Wang, Guang

AU - Liu, Jia

AU - Gao, Lin-rui

AU - Liu, Meng

AU - Wang, Chao-Jie

AU - Chuai, Manli

AU - Bao, Yongping

AU - Li, Ge

AU - Li, Rui-Man

AU - Zhang, Yu

AU - Yang, Xuesong

N1 - Funding: NSFC; Science and Technology Planning Project of Guangdong Province; Science and Technology Program of Guangzhou, Guangdong National Science Foundation

PY - 2018/12

Y1 - 2018/12

N2 - Background: Cytotoxicity and inflammation-associated toxic responses could be induced by bacterial lipopolysaccharides (LPS) in vitro and in vivo respectively. However, the mechanism involved in LPS-induced cardiac malformation in prenatal fetus is still unknown.Methods and results: In this study, we demonstrated that LPS was induced in gut microbiota imbalance mice, and next, LPS exposure during gastrulation in the chick embryo increased the incidence of cardia bifida. Gene transfection and tissue transplantation trajectory indicated that LPS exposure restricted the cell migration of cardiac progenitors to primary heart field in gastrula chick embryos. In vitro explant allograft of GFP-labeled anterior primitive streak demonstrated that LPS treatments could inhibit cell migration. A similar observation was also obtained from the cell migration assay of scratch wounds using primary culture of cardiomyocytes or H9c2 cells. In the embryos exposed to LPS, expressions of Nkx2.5 and GATA5 were disturbed. These genes are associated with cardiomyocyte differentiation when heart tube fusion occurs. Furthermore, pHIS3, C-caspase3 immunohistological staining indicated that cell proliferation decreased, cell apoptosis increased in the heart tube of chick embryo. Meanwhile, in vivo, pHIS3 immunohistological staining and Hochest/PI staining also draw the similar conclusions. The LPS exposure also caused the production of excess ROS, which might damage the cardiac precursor cells of developing embryos. At last, we showed that LPS-induced cardia bifida could be partially rescued through the addition of antioxidants.Conclusions: Together, these results reveal that excess ROS generation is involved in the LPS-induced defects in heart tube during chick embryo development. This article is protected by copyright. All rights reserved.

AB - Background: Cytotoxicity and inflammation-associated toxic responses could be induced by bacterial lipopolysaccharides (LPS) in vitro and in vivo respectively. However, the mechanism involved in LPS-induced cardiac malformation in prenatal fetus is still unknown.Methods and results: In this study, we demonstrated that LPS was induced in gut microbiota imbalance mice, and next, LPS exposure during gastrulation in the chick embryo increased the incidence of cardia bifida. Gene transfection and tissue transplantation trajectory indicated that LPS exposure restricted the cell migration of cardiac progenitors to primary heart field in gastrula chick embryos. In vitro explant allograft of GFP-labeled anterior primitive streak demonstrated that LPS treatments could inhibit cell migration. A similar observation was also obtained from the cell migration assay of scratch wounds using primary culture of cardiomyocytes or H9c2 cells. In the embryos exposed to LPS, expressions of Nkx2.5 and GATA5 were disturbed. These genes are associated with cardiomyocyte differentiation when heart tube fusion occurs. Furthermore, pHIS3, C-caspase3 immunohistological staining indicated that cell proliferation decreased, cell apoptosis increased in the heart tube of chick embryo. Meanwhile, in vivo, pHIS3 immunohistological staining and Hochest/PI staining also draw the similar conclusions. The LPS exposure also caused the production of excess ROS, which might damage the cardiac precursor cells of developing embryos. At last, we showed that LPS-induced cardia bifida could be partially rescued through the addition of antioxidants.Conclusions: Together, these results reveal that excess ROS generation is involved in the LPS-induced defects in heart tube during chick embryo development. This article is protected by copyright. All rights reserved.

KW - Lipopolysaccharides

KW - Chick Embryo

KW - Reactive oxygen species

KW - Heart Tube

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DO - 10.1002/jcp.26175

M3 - Article

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