Expression of corticotropin-releasing hormone receptor type-1 in intrahepatic cholestatic placental tissue.
- VernacularTitle:妊娠肝内胆汁淤积症患者胎盘促肾上腺皮质激素释放激素受体CRHR-1的表达
- Author:
Zheng-fei LIU
1
;
Mao-mao HE
;
Fan ZHOU
;
Bing-xin GAO
;
Xiao-dong WANG
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Case-Control Studies; Cholestasis, Intrahepatic; metabolism; Female; Humans; Liver Cirrhosis, Biliary; metabolism; Placenta; metabolism; Pregnancy; Pregnancy Complications; metabolism; Receptors, Corticotropin-Releasing Hormone; metabolism
- From: Chinese Journal of Hepatology 2013;21(5):381-384
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the expression level of corticotropin-releasing hormone receptor type-1 (CRHR-1) in intrahepatic cholestatic placental (ICP) tissue.
METHODSHuman placental samples were collected from 10 ICP patients and 10 healthy controls after parturition at 37-40 weeks of gestation. CRHR-1 protein and mRNA expression was assessed by western blotting and nested-real-time fluorescence quantitative PCR, respectively. Normally distributed data were summarized as mean +/- standard deviation, and intergroup comparisons were made by two-tailed Student's t-test. Non-normally distributed data were presented as median with interquartile range, and intergroup comparisons were made by Wilcoxon test. For all statistical analyses, a two-tailed P-value of less than 0.05 was considered statistically significant.
RESULTSThe CRHR-1 fluorescence intensity was lower in ICP tissues (1.55 +/- 0.28) than in placental tissues from healthy controls (1.60 +/- 0.37), but the difference did not reach statistical significance (t = 0.349, P = 0.732). The CRHR-1 mRNA content was slightly higher in the ICP tissues [0.139(0.268)] than in the placental tissues from healthy controls [0.031(0.245)], but the difference did not reach statistical significance (t = 1.504, P = 0.136).
CONCLUSIONCRHR-1 expression is decreased in ICP tissues, which may lead to a smaller volume of placental lobular villi vessels and restrict the CRH positive feedback loop, ultimately promoting acute hypoxic stress and possible harm to the fetus.