Long-term cardiovascular disorders in the STOX1 mouse model of preeclampsia

Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequen...

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Published in:Scientific reports Vol. 9; no. 1; pp. 11918 - 13
Main Authors: Miralles, Francisco, Collinot, Hélène, Boumerdassi, Yasmine, Ducat, Aurélien, Duché, Angéline, Renault, Gilles, Marchiol, Carmen, Lagoutte, Isabelle, Bertholle, Céline, Andrieu, Muriel, Jacques, Sébastien, Méhats, Céline, Vaiman, Daniel
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 15.08.2019
Nature Publishing Group
Subjects:
45/61
59
631/443/592/1540
631/443/592/75/243/793
64/60
Animals
Body Weight
Cardiovascular Diseases - blood
Cardiovascular Diseases - diagnostic imaging
Cardiovascular Diseases - etiology
Cardiovascular Diseases - genetics
Cardiovascular system
Carrier Proteins - metabolism
Cellular stress response
Chemokines
CXCL11 protein
CXCL13 protein
CXCL16 protein
Cytokines - metabolism
Deregulation
Disease Models, Animal
Doppler effect
Endothelial cells
Endothelial Cells - metabolism
Female
Females
Fibrosis
Gene Expression Regulation
Heart
Histology
Humanities and Social Sciences
Hypertrophy
Interleukin 10
Interleukin 16
Interleukin 2
Interleukin 4
Interleukin 6
Life Sciences
multidisciplinary
Myocardium - pathology
Organ Size
Pre-eclampsia
Pre-Eclampsia - blood
Pre-Eclampsia - pathology
Preeclampsia
Pregnancy
Reproductive Biology
Rodents
Science
Science (multidisciplinary)
Transcription, Genetic
Ultrasonic imaging
Ultrasound
Ventricle
ISSN:2045-2322, 2045-2322
Online Access:Get full text
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Abstract Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequences on the maternal cardiovascular system. Ultrasonography parameters were analyzed in mice before pregnancy and at 3 and 6 months post-pregnancy. At 6 months post-pregnancy, cardiac stress test induced by dobutamine injection revealed an abnormal ultrasonography Doppler profile in mice with previous PE. Eight months post-pregnancy, the heart, endothelial cells (ECs) and plasma of females were analyzed and compared to controls. The heart of mice with PE showed left-ventricular hypertrophy associated with altered histology (fibrosis). Transcriptomic analysis revealed the deregulation of 1149 genes in purified ECs and of 165 genes in the hearts, many being involved in heart hypertrophy. In ECs, the upregulated genes were associated with inflammation and cellular stress. Systems biology analysis identified interleukin 6 (IL-6) as a hub gene connecting these pathways. Plasma profiling of 33 cytokines showed that, 8 of them (Cxcl13, Cxcl16, Cxcl11, IL-16, IL-10, IL-2, IL-4 and Ccl1) allowed to discriminate mice with previous PE from controls. Thus, PE triggers female long-term CV consequences on the STOX1 mouse model.
AbstractList Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequences on the maternal cardiovascular system. Ultrasonography parameters were analyzed in mice before pregnancy and at 3 and 6 months post-pregnancy. At 6 months post-pregnancy, cardiac stress test induced by dobutamine injection revealed an abnormal ultrasonography Doppler profile in mice with previous PE. Eight months post-pregnancy, the heart, endothelial cells (ECs) and plasma of females were analyzed and compared to controls. The heart of mice with PE showed left-ventricular hypertrophy associated with altered histology (fibrosis). Transcriptomic analysis revealed the deregulation of 1149 genes in purified ECs and of 165 genes in the hearts, many being involved in heart hypertrophy. In ECs, the upregulated genes were associated with inflammation and cellular stress. Systems biology analysis identified interleukin 6 (IL-6) as a hub gene connecting these pathways. Plasma profiling of 33 cytokines showed that, 8 of them (Cxcl13, Cxcl16, Cxcl11, IL-16, IL-10, IL-2, IL-4 and Ccl1) allowed to discriminate mice with previous PE from controls. Thus, PE triggers female long-term CV consequences on the STOX1 mouse model.
Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequences on the maternal cardiovascular system. Ultrasonography parameters were analyzed in mice before pregnancy and at 3 and 6 months post-pregnancy. At 6 months post-pregnancy, cardiac stress test induced by dobutamine injection revealed an abnormal ultrasonography Doppler profile in mice with previous PE. Eight months post-pregnancy, the heart, endothelial cells (ECs) and plasma of females were analyzed and compared to controls. The heart of mice with PE showed left-ventricular hypertrophy associated with altered histology (fibrosis). Transcriptomic analysis revealed the deregulation of 1149 genes in purified ECs and of 165 genes in the hearts, many being involved in heart hypertrophy. In ECs, the upregulated genes were associated with inflammation and cellular stress. Systems biology analysis identified interleukin 6 (IL-6) as a hub gene connecting these pathways. Plasma profiling of 33 cytokines showed that, 8 of them (Cxcl13, Cxcl16, Cxcl11, IL-16, IL-10, IL-2, IL-4 and Ccl1) allowed to discriminate mice with previous PE from controls. Thus, PE triggers female long-term CV consequences on the STOX1 mouse model.Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequences on the maternal cardiovascular system. Ultrasonography parameters were analyzed in mice before pregnancy and at 3 and 6 months post-pregnancy. At 6 months post-pregnancy, cardiac stress test induced by dobutamine injection revealed an abnormal ultrasonography Doppler profile in mice with previous PE. Eight months post-pregnancy, the heart, endothelial cells (ECs) and plasma of females were analyzed and compared to controls. The heart of mice with PE showed left-ventricular hypertrophy associated with altered histology (fibrosis). Transcriptomic analysis revealed the deregulation of 1149 genes in purified ECs and of 165 genes in the hearts, many being involved in heart hypertrophy. In ECs, the upregulated genes were associated with inflammation and cellular stress. Systems biology analysis identified interleukin 6 (IL-6) as a hub gene connecting these pathways. Plasma profiling of 33 cytokines showed that, 8 of them (Cxcl13, Cxcl16, Cxcl11, IL-16, IL-10, IL-2, IL-4 and Ccl1) allowed to discriminate mice with previous PE from controls. Thus, PE triggers female long-term CV consequences on the STOX1 mouse model.
Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here, we mated wild-type female mice of the FVB/N strain to STOX1A-overexpressing mice to mimic severe PE and investigated the long-term consequences on the maternal cardiovascular system. Ultrasonography parameters were analyzed in mice before pregnancy and at 3 and 6 months post-pregnancy. At 6 months post-pregnancy, cardiac stress test induced by dobutamine injection revealed an abnormal ultrasonography Doppler profile in mice with previous PE. Eight months post-pregnancy, the heart, endothelial cells (ECs) and plasma of females were analyzed and compared to controls. The heart of mice with PE showed left-ventricular hypertrophy associated with altered histology (fibrosis). Transcriptomic analysis revealed the deregulation of 1149 genes in purified ECs and of 165 genes in the hearts, many being involved in heart hypertrophy. In ECs, the upregulated genes were associated with inflammation and cellular stress. Systems biology analysis identified interleukin 6 (IL-6) as a hub gene connecting these pathways. Plasma profiling of 33 cytokines showed that, 8 of them (Cxcl13, Cxcl16, Cxcl11, IL-16, IL-10, IL-2, IL-4 and Ccl1) allowed to discriminate mice with previous PE from controls. Thus, PE triggers female long-term CV consequences on the STOX1 mouse model.
ArticleNumber 11918
Author Vaiman, Daniel
Marchiol, Carmen
Méhats, Céline
Ducat, Aurélien
Lagoutte, Isabelle
Jacques, Sébastien
Andrieu, Muriel
Duché, Angéline
Miralles, Francisco
Collinot, Hélène
Boumerdassi, Yasmine
Renault, Gilles
Bertholle, Céline
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PublicationTitle Scientific reports
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Snippet Adverse long-term cardiovascular (CV) consequences of PE are well established in women. However, the mechanism responsible for that risk remains unknown. Here,...
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StartPage 11918
SubjectTerms 45/61
59
631/443/592/1540
631/443/592/75/243/793
64/60
Animals
Body Weight
Cardiovascular Diseases - blood
Cardiovascular Diseases - diagnostic imaging
Cardiovascular Diseases - etiology
Cardiovascular Diseases - genetics
Cardiovascular system
Carrier Proteins - metabolism
Cellular stress response
Chemokines
CXCL11 protein
CXCL13 protein
CXCL16 protein
Cytokines - metabolism
Deregulation
Disease Models, Animal
Doppler effect
Endothelial cells
Endothelial Cells - metabolism
Female
Females
Fibrosis
Gene Expression Regulation
Heart
Histology
Humanities and Social Sciences
Hypertrophy
Interleukin 10
Interleukin 16
Interleukin 2
Interleukin 4
Interleukin 6
Life Sciences
multidisciplinary
Myocardium - pathology
Organ Size
Pre-eclampsia
Pre-Eclampsia - blood
Pre-Eclampsia - pathology
Preeclampsia
Pregnancy
Reproductive Biology
Rodents
Science
Science (multidisciplinary)
Transcription, Genetic
Ultrasonic imaging
Ultrasound
Ventricle
Title Long-term cardiovascular disorders in the STOX1 mouse model of preeclampsia
URI https://link.springer.com/article/10.1038/s41598-019-48427-3
https://www.ncbi.nlm.nih.gov/pubmed/31417152
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https://pubmed.ncbi.nlm.nih.gov/PMC6695383
Volume 9
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