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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2008-7-9
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pubmed:abstractText |
We previously demonstrated that several clinically utilized volatile anesthetics including sevoflurane protected against renal ischemia-reperfusion (IR) injury by reducing necrosis and inflammation in vivo. We also demonstrated that volatile anesthetics produced direct anti-necrotic and anti-inflammatory effects in cultured renal tubules via mechanisms involving the externalization of phosphatidylserine and subsequent release of transforming growth factor (TGF)-beta1. In this study, we tested the hypothesis that volatile anesthetic-mediated renal protection requires TGF-beta1 and SMAD3 signaling in vivo. We subjected TGF-beta1+/+, TGF-beta1+/-, SMAD3+/+, or SMAD3-/- mice to renal IR under anesthesia with pentobarbital sodium or with sevoflurane. Although TGF-beta1+/+ and SMAD3+/+ mice were significantly protected against renal IR injury under sevoflurane anesthesia with reduced necrosis and inflammation, TGF-beta1+/- mice and SMAD3-/- mice were not protected against renal IR with sevoflurane. Furthermore, a neutralizing TGF-beta1 antibody blocked renal protection with sevoflurane in TGF-beta1+/+ mice. Sevoflurane caused nuclear translocation of SMAD3 and reduced the TNF-alpha-induced nuclear translocation of NF-kappaB in primary cultures of proximal tubules from TGF-beta1+/+ but not in TGF-beta1+/- mice. Finally, sevoflurane protected against necrosis induced with hydrogen peroxide in primary cultures of proximal tubules from TGF-beta1+/+ mice or SMAD3+/+ mice but not in proximal tubules from TGF-beta1+/- or SMAD3-/- mice. Therefore, we demonstrate in this study that sevoflurane-mediated renal protection in vivo requires the TGF-beta1-->SMAD3 signaling pathway.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-10064594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-10344355,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-10611754,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-10648114,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-10811223,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-11483996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-11781349,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-11842088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-12235115,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-12388399,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-12957874,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-14600029,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-14694162,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-14760876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-15365924,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-15461705,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-15564938,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-15661897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-16478975,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-17413392,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-17596528,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-17622749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-7826627,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-8618872,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-9054745,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-9466984,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18434384-9853246
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anesthetics, Inhalation,
http://linkedlifedata.com/resource/pubmed/chemical/Methyl Ethers,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Smad3 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Smad3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1,
http://linkedlifedata.com/resource/pubmed/chemical/sevoflurane
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1931-857X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
295
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F128-36
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pubmed:dateRevised |
2011-4-28
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pubmed:meshHeading |
pubmed-meshheading:18434384-Anesthetics, Inhalation,
pubmed-meshheading:18434384-Animals,
pubmed-meshheading:18434384-Cells, Cultured,
pubmed-meshheading:18434384-Kidney Diseases,
pubmed-meshheading:18434384-Kidney Medulla,
pubmed-meshheading:18434384-Methyl Ethers,
pubmed-meshheading:18434384-Mice,
pubmed-meshheading:18434384-NF-kappa B,
pubmed-meshheading:18434384-RNA, Messenger,
pubmed-meshheading:18434384-Reperfusion Injury,
pubmed-meshheading:18434384-Smad3 Protein,
pubmed-meshheading:18434384-Transforming Growth Factor beta1
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pubmed:year |
2008
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pubmed:articleTitle |
Sevoflurane protects against renal ischemia and reperfusion injury in mice via the transforming growth factor-beta1 pathway.
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pubmed:affiliation |
Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY 10032-3784, USA. tl128@columbia.edu
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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