title: Effects of a restricted fetal growth environment on human kidney morphology, cell apoptosis and gene expression.
abstract: OBJECTIVE
  Kidney development is key to the onset of hypertension and cardiovascular diseases in adults, and in the fetal stage will be impaired by a lack of nutrients in utero in animal models. However, few human studies have been performed.
  
  
  METHODS
  Kidney samples from fetuses in a fetal growth restriction (FGR) environment were collected and the morphological characteristics were observed. Potentially molecular mechanisms were explored by analyzing apoptosis and kidney-development related gene expression.
  
  
  RESULTS
  The results indicated that no malformations were observed in the kidney samples of the FGR group, but the mean kidney weight and volume were significantly decreased. Moreover, the ratio of apoptotic cells and Bax-positive cells was increased and the ratio of Bcl-2-positive cells was decreased in the FGR group, indicating potential apoptosis induction under an in utero FGR environment. Finally, aberrant expression of renin and angiotensinogen indicated potential kidney functional abnormalities in the FGR group.
  
  
  CONCLUSIONS
  Our study suggested increased apoptosis and decreased renin and angiotensinogen expression during human kidney development in an FGR environment. The current results will be helpful to further explore the molecular mechanism of FGR and facilitate future studies of hypertension and cardiovascular diseases and the establishment of preventive methods.
authors.affiliation: Department of Obstetrics, Tianjin Central Hospital of Gynecology Obstetrics, China.
authors.forename: Yan-Ping
authors.initials: YP
authors.lastname: Wang
authors.affiliation: Department of Obstetrics, Tianjin Central Hospital of Gynecology Obstetrics, China chenshutj@126.com.
authors.forename: Xu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Obstetrics, Tianjin Central Hospital of Gynecology Obstetrics, China.
authors.forename: Zhi-Kun
authors.initials: ZK
authors.lastname: Zhang
authors.affiliation: Department of Obstetrics, Tianjin Central Hospital of Gynecology Obstetrics, China.
authors.forename: Hong-Yan
authors.initials: HY
authors.lastname: Cui
authors.affiliation: Department of Obstetrics, Tianjin Central Hospital of Gynecology Obstetrics, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.affiliation: Department of Obstetrics, Tianjin Central Hospital of Gynecology Obstetrics, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000328:Adult; D000808:Angiotensinogen / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis / Q000235:genetics*; D001724:Birth Weight; D016022:Case-Control Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics* / Q000473:pathology*; D005333:Fetus / Q000473:pathology; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D007668:Kidney / Q000196:embryology* / Q000378:metabolism / Q000473:pathology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012083:Renin / Q000235:genetics / Q000378:metabolism; D055815:Young Adult
chemical_list: D012333:RNA, Messenger; D000808:Angiotensinogen; D012083:Renin
keywords: Renin–angiotensinogen system; apoptosis; fetal kidney development; gestation; uterine environment