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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Vydáno v:	Scientific reports Ročník 9; číslo 1; s. 11918 - 13
Hlavní autoři:	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
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 15.08.2019 Nature Publishing Group
Témata:	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
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Shrnutí:	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.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 PMCID: PMC6695383
ISSN:	2045-2322 2045-2322
DOI:	10.1038/s41598-019-48427-3