Effects of a restricted fetal growth environment on human kidney morphology, cell apoptosis and gene expression.
J Renin Angiotensin Aldosterone Syst
; 16(4): 1028-35, 2015 Dec.
Article
em En
| MEDLINE
| ID: mdl-25271252
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.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Apoptose
/
Regulação da Expressão Gênica no Desenvolvimento
/
Retardo do Crescimento Fetal
/
Rim
Tipo de estudo:
Observational_studies
/
Prognostic_studies
Limite:
Adult
/
Female
/
Humans
/
Pregnancy
Idioma:
En
Revista:
J Renin Angiotensin Aldosterone Syst
Assunto da revista:
FISIOLOGIA
Ano de publicação:
2015
Tipo de documento:
Article
País de afiliação:
China