The reduction of Na/H exchanger-3 protein and transcript expression in acute ischemia-reperfusion injury is mediated by extractable tissue factor(s).

Ischemic renal injury is a formidable clinical problem, the pathophysiology of which is incompletely understood. As the Na/H exchanger-3 (NHE3) mediates the bulk of apical sodium transport and a significant fraction of oxygen consumption in the proximal tubule, we examined mechanisms by which ischem...

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Publicado en:Kidney International Vol. 80; no. 8; pp. 822 - 832
Autores principales: Di Sole F, Hu MC, Zhang J, Babich V, Bobulescu IA, Shi M, McLeroy P, Rogers TE, Moe OW, Di Sole, Francesca, Hu, Ming-Chang, Zhang, Jianning, Babich, Victor, Bobulescu, I Alexandru, Shi, Mingjun, McLeroy, Paul, Rogers, Thomas E, Moe, Orson W, Sole, Francesca Di, Francesca Di, Sole
Formato: research Journal Article
Publicado: Elsevier B.V. Oct2011
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Oct2011
      vid: 80
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      pub: Elsevier B.V.
      place: Philadelphia, Pennsylvania
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        10.1038/ki.2011.229
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        atl: The reduction of Na/H exchanger-3 protein and transcript expression in acute ischemia-reperfusion injury is mediated by extractable tissue factor(s).
      aug:
        au:
          Di Sole F
          Hu MC
          Zhang J
          Babich V
          Bobulescu IA
          Shi M
          McLeroy P
          Rogers TE
          Moe OW
          Di Sole, Francesca
          Hu, Ming-Chang
          Zhang, Jianning
          Babich, Victor
          Bobulescu, I Alexandru
          Shi, Mingjun
          McLeroy, Paul
          Rogers, Thomas E
          Moe, Orson W
          Sole, Francesca Di
          Francesca Di, Sole
        affil: Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8885, USA
      sug:
        subj:
          Reperfusion Injury Metabolism
          Biological Transport Physiology
          Thromboplastin Physiology
          Acute Disease
          Animals
          Cells
          Immunohistochemistry
          Mammals
          RNA Analysis
          Rats
          Biological Transport
      ab: Ischemic renal injury is a formidable clinical problem, the pathophysiology of which is incompletely understood. As the Na/H exchanger-3 (NHE3) mediates the bulk of apical sodium transport and a significant fraction of oxygen consumption in the proximal tubule, we examined mechanisms by which ischemia-reperfusion affects the expression of NHE3. Ischemia-reperfusion dramatically decreased NHE3 protein and mRNA (immunohistochemistry, immunoblot, and RNA blot) in rat kidney cortex and medulla. The decrease in NHE3 protein was uniform throughout all tubules, including those appearing morphologically intact. In the kidney cortex, a decrease in NHE3 surface protein preceded that of NHE3 total protein and mRNA. Kidney homogenates from rats exposed to mild renal ischemia-reduced cell surface NHE3 protein expression in opossum kidney cells in vitro, whereas homogenates from animals with moderate-to-severe ischemia reduced both total NHE3 protein and mRNA. The decrease in total NHE3 protein was dependent on the proteasomal degradation associated with NHE3 ubiquitylation measured by coimmunoprecipitation. The transferable factor(s) from the ischemic homogenate that reduce NHE3 expression were found to be heat sensitive and to be associated with a lipid-enriched fraction, and did not include regulatory RNAs. Thus, transferable factor(s) mediate the ischemia-reperfusion injury-induced decrease in NHE3 of the kidney.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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