Pharmacology: 17β-estradiol induces gastrointestinal motility disorder by decreasing CPI-17 phosphorylation via changes in Rho-family G-protein Rnd expression in small intestine
-
- SHIMOMURA Aya
- Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo
-
- OHAMA Takashi
- Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo
-
- HORI Masatoshi
- Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo
-
- OZAKI Hiroshi
- Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo
書誌事項
- タイトル別名
-
- 17.BETA.-Estradiol Induces Gastrointestinal Motility Disorder by Decreasing CPI-17 Phosphorylation Via Changes in Rho-Family G-Protein Rnd Expression in Small Intestine
- Pharmacology 17 v estradiol induces gastrointestinal motility disorder by decreasing CPI 17 phosphorylation via changes in Rho family G protein Rnd expression in small intestine
この論文をさがす
抄録
In the present study, we investigated the long-term effects of 17β-estradiol on the motility of small intestine in in vitro organ culture and in vivo treatment studies. When rat ileal circular smooth muscle tissues were cultured with 17β-estradiol (0.1 and 1 μM) for 5 days, carbachol-induced contraction was inhibited. In ileal tissue isolated from ovariectomized rat treated with 17β-estradiol (200 μg/kg/day s.c. for 3 days), carbachol-induced contraction was also impaired. Both in vitro and in vivo, 17β-estradiol treatment upregulated heat shock protein 27 (HSP27) expression, indicating the activation of estrogen receptor in the intestinal smooth muscle. 17β-estradiol did not change protein expression levels of RhoA and RhoA-associated coiled coil-forming serine/threonine kinases (ROCKs); however, it upregulated Rnd2 and Rnd3, Rho-family G-proteins that counteract the functions of RhoA, both in vitro and in vivo. In organ culture, treatment of ileal tissue with 17β-estradiol greatly suppressed the carbachol-induced increase in phosphorylation at Thr38 in CPI-17 without altering total CPI-17 protein expression. These results suggest that 17β-estradiol upregulates Rnd expression to inhibit the RhoA-mediated Ca2+ sensitization of contractile mechanisms, which are mediated by CPI-17 phosphorylation in ileal smooth muscle. This mechanism may contribute to the intestinal motility disorder occurring in gender-dependent bowel diseases.<br>
収録刊行物
-
- The Journal of Veterinary Medical Science
-
The Journal of Veterinary Medical Science 71 (12), 1591-1597, 2009
公益社団法人 日本獣医学会
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1390001206430041344
-
- NII論文ID
- 130000149985
-
- NII書誌ID
- AA10796138
-
- ISSN
- 13477439
- 09167250
-
- NDL書誌ID
- 10530525
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- CiNii Articles
- KAKEN
-
- 抄録ライセンスフラグ
- 使用不可