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Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt.

Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt. Research Abstract Details 

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  • Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt. Abstract Text:

    rui zengRui Zeng,ying yaoYing Yao,min hanMin Han,xiaoqin zhaoXiaoqin Zhao,xiao-cheng liuXiao-Cheng Liu,juncheng weiJuncheng Wei,yun luoYun Luo,juan zhangJuan Zhang,jianfeng zhouJianfeng Zhou,shixuan wangShixuan Wang,ding maDing Ma,gang xuGang Xu,rui zengRui Zeng,ying yaoYing Yao,min hanMin Han,xiaoqin zhaoXiaoqin Zhao,xiao-cheng liuXiao-Cheng Liu,juncheng weiJuncheng Wei,yun luoYun Luo,juan zhangJuan Zhang,jianfeng zhouJianfeng Zhou,shixuan wangShixuan Wang,ding maDing Ma,gang xuGang Xu,

    Chronic hypoxia in the renal parenchyma is thought to induce epithelial-to-mesenchymal transition (EMT), leading to fibrogenesis and ultimately end-stage renal failure. Biliverdin reductase, recently identified as a serine/threonine/tyrosine kinase that may activate phosphatidylinositol 3-kinase (PI3K) and Akt, is upregulated in response to reactive oxygen species that may accompany hypoxia. We investigated this potential role of biliverdin reductase in hypoxia-induced renal tubular EMT. Expression of biliverdin reductase was upregulated in a human proximal tubule cell line (HK-2) cultured in hypoxic conditions (1% O2), and this was accompanied by reduced expression of E-cadherin and increased expression of the mesenchymal marker vimentin. Inhibiting PI3K reversed these changes, consistent with EMT. In normoxic conditions, overexpression of biliverdin reductase promoted similar characteristics of EMT, which were also reversed by inhibiting PI3K. Furthermore, using small interfering RNA (siRNA) to knockdown biliverdin reductase, we demonstrated that the enzyme associates with phosphorylated Akt and mediates the hypoxia-induced EMT phenotype. In vivo, expression of biliverdin reductase increased in the tubular epithelia of 5/6-nephrectomized rats, and immunohistochemistry of serial sections demonstrated similar localization of phosphorylated Akt and biliverdin reductase. In conclusion, biliverdin reductase mediates hypoxia-induced EMT through a PI3K/Akt-dependent pathway.

    Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt. Publishing Authors By Initials

    r zengR Zeng,y yaoY Yao,m hanM Han,x zhaoX Zhao,xc liuXC Liu,j weiJ Wei,y luoY Luo,j zhangJ Zhang,j zhouJ Zhou,s wangS Wang,d maD Ma,g xuG Xu,r zengR Zeng,y yaoY Yao,m hanM Han,x zhaoX Zhao,xc liuXC Liu,j weiJ Wei,y luoY Luo,j zhangJ Zhang,j zhouJ Zhou,s wangS Wang,d maD Ma,g xuG Xu,

    For similar abstracts research abstracts see: abstracts research

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    Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of the American Society of Nephrology : JA

    VOLUME: 19

    Page Numbers: 380-7

    Journal Abbreviation: J. Am. Soc. Nephrol.

    ISSN: 1533-3450

    DAY: 9

    MONTH: 01

    YEAR: 2008

    Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt. Information

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    LANGUAGE: eng

    NlmUniqueID: 9013836

    Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt. Keywords Mesh Terms:

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    Grant and Affiliation Information for Biliverdin reductase mediates hypoxia-induced EMT via PI3-kinase and Akt.

    AFFILIATION: Division of Nephrology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, People's Republic of China.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: J Am Soc Nephrol

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