Morphologic effects of the epithelial ion channels on the mouse uterus : differences between raloxifene analogue (LY117018) and estradiol treatments.
American Journal of Obstetrics & Gynecology Volume 199 Issue 4
Page 363.e1-363.e6
published_at 2008-10
アクセス数 : 945 件
ダウンロード数 : 235 件
今月のアクセス数 : 4 件
今月のダウンロード数 : 3 件
この文献の参照には次のURLをご利用ください : https://ir.lib.hiroshima-u.ac.jp/00025934
File |
AmJObstetGynecol_199_363.pdf
516 KB
種類 :
fulltext
|
Title ( eng ) |
Morphologic effects of the epithelial ion channels on the mouse uterus : differences between raloxifene analogue (LY117018) and estradiol treatments.
|
Creator | |
Source Title |
American Journal of Obstetrics & Gynecology
|
Volume | 199 |
Issue | 4 |
Start Page | 363.e1 |
End Page | 363.e6 |
Abstract |
Objectives: Estrogen regulates the expression of epithelial Na+ channel (ENaC) and cystic fibrosis transmembrane conductance regulator (CFTR). Our purpose was to assess the effects of raloxifene analogue LY117018 on the expression of ENaC and CFTR in ovariectomized mice.
Study design: Three groups of 5 female ovariectomized mice were treated with 17β-estradiol benzoate (E2), LY117018 (LY), or vehicle, respectively, for 4 to 12 weeks. Effects on the mRNA expression levels of ENaC and CFTR channels in the uterus were studied using real-time reverse transcriptase-polymerase chain reaction. Results: E2 treatment induced CFTR expression, repressed ENaC expression and resulted in fluid accumulation in the uterus. In contrast, LY induced CFTR expression, did not repress ENaC expression, and caused no fluid accumulation. Conclusions: Estradiol and LY117018 differentially regulate the expression of CFTR and ENaC in ovariectomized mouse uterus. This finding suggests that uterine fluid accumulation can be controlled mainly by targeting the ENaC. |
Keywords |
CFTR
ENaC
Fluid accumulation
Mouse uterus
SERM
|
NDC |
Medical sciences [ 490 ]
|
Language |
eng
|
Resource Type | journal article |
Publisher |
Mosby
Elsevier
|
Date of Issued | 2008-10 |
Rights |
Copyright (c) 2008 Mosby, Inc.
|
Publish Type | Author’s Original |
Access Rights | open access |
Source Identifier |
[ISSN] 0002-9378
[DOI] 10.1016/j.ajog.2008.03.047
[NCID] AA00520844
[DOI] http://dx.doi.org/10.1016/j.ajog.2008.03.047
|