Renal developmental retardation and the underlying mechanism induced by prenatal caffeine exposure in female fetal rats
10.3969/j.issn.1001-1978.2018.02.014
- VernacularTitle:孕期咖啡因暴露所致雌性子代胎鼠肾脏宫内发育迟缓及其发生机制
- Author:
Yang WAN
1
;
Ying AO
;
Bin LI
;
Ying XIONG
;
Zhao-Xia SUN
;
Shuang-Shuang HU
;
Hui WANG
Author Information
1. 武汉大学基础医学院药理学系
- Keywords:
prenatal caffeine exposure;
intrauterine growth retardation;
glucocorticoid;
fetal renal dysplasia;
angiotensin Ⅱ receptor type 1/2;
glial-cell-line-derived neurotrophic factor/ tyrosine kinase receptor signaling pathway
- From:
Chinese Pharmacological Bulletin
2018;34(2):213-219
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the effects of prenatal caf-feine exposure (PCE) on fetal renal growth retardation and corticosterone on the gene expression of metanephric mesenchyme stem cells.Methods Pregnant Wistar rats were administered with caffeine (30,120 mg ·kg-1) from gestational day 9 to 20.Female fetal kidney samples were collected for morphological observation and gene expression examination.The metanephric mesenchyme stem cells were harvested for cell culture,and renal related genes were detected after the treatment of corticosterone with different concentrations (250,500,1 000 μg · L-1) for 24 hours.Results Compared with the control group,the fetal kidneys in the PCE group displayed an enlarged Bowman's space and a shrunken glomerular tuft,accompanied with the repression of the gene expression of glial-cell-line-derived neurotrophic factor/tyrosine kinase receptor (GDNF/c-Ret) signaling pathway.The GDNF/c-Ret signaling pathway and angiotensin Ⅱ receptor type 1 (AT1R)/AT2R expression of metanephric mesenchyme stem cells also decreased in corticosterone groups.Conclusions PCE may induce dysplasia of female fetal kidneys.The potential mechanism is related to the repression of the gene expression of AT1R/AT2R and GDNF/c-Ret signaling pathway by PCE mediated by corticosterone in utero.
