title: Maternal high-salt intake during pregnancy reprogrammed renin-angiotensin system-mediated cardiomyocyte apoptosis in the adult offspring heart.
abstract: OBJECTIVE
  Excess salt intake during pregnancy may alter fetal organ structures and functions leading to increased risks in the development of cardiovascular diseases in later life. The present study determined whether and how the prenatal high-salt (HS) diets affect renin-angiotensin system (RAS) that may mediate cardiac cell death.
  
  
  RESULTS
  Angiotensin II receptors, AT1 and AT2, protein expression was increased in the myocardium of the offspring exposed to prenatal HS; apoptotic cells appeared in the myocardium of the adult offspring. Mitochondrion was isolated in cell experiments, and the data showed cardiomyocyte apoptosis requiring cytochrome C release. Pretreating H9C2 cells with AT2 agonist CGP42112A induced cell apoptosis in DNA fragments and activated caspase 3. CGP42112A increased mitochondrion cytochrome C release and apoptosis in the cells.
  
  
  CONCLUSIONS
  Both in vitro and in vivo study demonstrated that cardiomyocyte apoptosis was related to AT2 activation. Prenatal HS diets may reprogram RAS that mediates apoptosis in the offspring myocardium, and AT2 may contribute to cardiomyocyte apoptosis via the cytochrome C release pathway.
authors.affiliation: 1Institute for Fetology, The First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Juanxiu
authors.initials: J
authors.lastname: Lv
authors.forename: Peiwen
authors.initials: P
authors.lastname: Zhang
authors.forename: Yujuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Hanzhe
authors.initials: H
authors.lastname: Kuang
authors.forename: Li
authors.initials: L
authors.lastname: Cao
authors.forename: Conglong
authors.initials: C
authors.lastname: Wu
authors.forename: Lin
authors.initials: L
authors.lastname: Jiang
authors.forename: Dawei
authors.initials: D
authors.lastname: Li
authors.forename: Caiping
authors.initials: C
authors.lastname: Mao
authors.forename: Zhice
authors.initials: Z
authors.lastname: Xu
mesh_terms: D000367:Age Factors; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002460:Cell Line; D045304:Cytochromes c / Q000378:metabolism; D004789:Enzyme Activation; D005260:Female; D039382:Maternal Nutritional Physiological Phenomena; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D009842:Oligopeptides / Q000494:pharmacology; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000819:agonists / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*
chemical_list: D009842:Oligopeptides; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D017673:Sodium Chloride, Dietary; C060894:CGP 42112A; D045304:Cytochromes c; C505410:Casp3 protein, rat; D053148:Caspase 3
keywords: angiotensin receptors; apoptosis; high salt; offspring heart