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学科主题: 基础医学
题名:
Aquaporin-2 regulates cell volume recovery via tropomyosin
作者: Li, Yu-Hua1,2,3; Eto, Kayoko3; Horikawa, Saburo4; Uchida, Shinichi3; Sasaki, Sei3; Li, Xue-Jun1,2; Noda, Yumi3
关键词: Aquaporin ; Cell volume regulation ; Collecting duct cells ; Osmolality ; Tropomyosin
刊名: INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
发表日期: 2009-12-01
DOI: 10.1016/j.biocel.2009.07.017
卷: 41, 期:12, 页:2466-2476
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]: Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]: WATER CHANNEL AQUAPORIN-2 ; F-ACTIN ; COLLECTING DUCT ; TERMINAL TAIL ; RENAL-CELLS ; TRAFFICKING ; PHOSPHORYLATION ; ACTIVATION ; BINDING ; AQP2
英文摘要:

Cell volume regulation is particularly important for kidney collecting duct cells. These cells are the site of water reabsorption regulated by vasopressin and aquaporin-2 (AQP2) trafficking to the apical membrane, and subject to changes in osmolality. Here, we examined the role of AQP2 in regulatory volume decrease (RVD), which is a cellular defensive process against hypotonic stress. Stable expression of AQP2 increases RVD in MDCK cells and its phosphorylation levels decrease during the RVD process. We then examined the involvement of AQP2 phosphorylation at serine 256 and serine 261 in RVD using cells stably expressing the phosphorylation mutants. Both S256A- and S256D-AQP2 decrease RVD compared to wild type (WT)-AQP2 although only S256A mutation decreases the initial osmotic swelling, indicating that AQP2-enhanced RVD is independent of osmotic swelling induced by the water permeability of AQP2. S261A and S261D mutations do not induce changes compared with WT-AQP2. These findings indicate that switching between phosphorylation and dephosphorylation at S256 is important for RVD. We previously reported that AQP2 interacts with tropomyosin 5b (TM5b), which regulates actin stability. AQP2 interactions with TM5b are rapidly increased by hypotonicity and then decreased, which are consistent with AQP2 phosphorylation levels. Knockdown and overexpression of TM5b show its essential role in WT-AQP2-enhanced RVD. RVD in S256A- and S256D-AQP2-expressing cells is not changed by TM5b knockdown or overexpression. The present study shows that AQP2 regulates RVD via TM5b and switching between phosphorylation and dephosphorylation at S256 in AQP2 is critical for this process. (C) 2009 Elsevier Ltd. All rights reserved.

语种: 英语
所属项目编号: 17GS0312
项目资助者: Japan Society for the Promotion of Science
WOS记录号: WOS:000272218400018
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66781
Appears in Collections:基础医学院_药理学系_期刊论文

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作者单位: 1.Peking Univ, Dept Pharmacol, Sch Basic Med Sci, Beijing 100191, Peoples R China
2.Peking Univ, State Key Lab Nat Biomimet Drugs, Sch Basic Med Sci, Beijing 100191, Peoples R China
3.Tokyo Med & Dent Univ, Dept Nephrol, Bunkyo Ku, Tokyo 1138519, Japan
4.Tokyo Med & Dent Univ, Div Pathophysiol, Med Res Inst, Bunkyo Ku, Tokyo 1138510, Japan

Recommended Citation:
Li, Yu-Hua,Eto, Kayoko,Horikawa, Saburo,et al. Aquaporin-2 regulates cell volume recovery via tropomyosin[J]. INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY,2009,41(12):2466-2476.
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