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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2002-9-12
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pubmed:abstractText |
Lung ischemia-reperfusion (I-R) is an important model of oxidant-mediated acute lung and vascular injury. Heme oxygenase-1 (HO-1) is a cytoprotective gene that is markedly induced by lung I-R injury. HO-1 mRNA is increased in mouse lung after 30 min of lung hilar clamping (ischemia) followed by 2-6 h of unclamping (reperfusion) compared with control mice. In a variety of vascular cell types, HO-1 mRNA is induced after 24 h of anoxia followed by 30 min-1 h of reoxygenation (A-R). Transfection studies reveal that the promoter and 5'-distal enhancer E1 are necessary and sufficient for increased HO-1 gene transcription after A-R. Immunoblotting studies show all three subfamilies of MAPKs (ERK, JNK, and p38) are activated by 15 min of reperfusion. We also demonstrate that HO-1 gene transcription after A-R involves ERK, JNK, and p38 MAPK pathways. Together, our data show that I-R not only induces HO-1 gene expression in mouse lungs and vascular cells but that gene transcription occurs via the promoter and E1 enhancer and involves upstream MAPK pathways.
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pubmed:grant |
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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/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Flavonoids,
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase (Decyclizing),
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase-1,
http://linkedlifedata.com/resource/pubmed/chemical/Hmox1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/PD 98059,
http://linkedlifedata.com/resource/pubmed/chemical/Pyridines,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/SB 203580,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1040-0605
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
283
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
L815-29
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12225959-Animals,
pubmed-meshheading:12225959-Aorta,
pubmed-meshheading:12225959-Cells, Cultured,
pubmed-meshheading:12225959-Enhancer Elements, Genetic,
pubmed-meshheading:12225959-Enzyme Inhibitors,
pubmed-meshheading:12225959-Flavonoids,
pubmed-meshheading:12225959-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:12225959-Heme Oxygenase (Decyclizing),
pubmed-meshheading:12225959-Heme Oxygenase-1,
pubmed-meshheading:12225959-Imidazoles,
pubmed-meshheading:12225959-Lung Diseases,
pubmed-meshheading:12225959-MAP Kinase Signaling System,
pubmed-meshheading:12225959-Membrane Proteins,
pubmed-meshheading:12225959-Mice,
pubmed-meshheading:12225959-Mitogen-Activated Protein Kinase 9,
pubmed-meshheading:12225959-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12225959-Muscle, Smooth, Vascular,
pubmed-meshheading:12225959-Mutagenesis,
pubmed-meshheading:12225959-Promoter Regions, Genetic,
pubmed-meshheading:12225959-Pulmonary Artery,
pubmed-meshheading:12225959-Pyridines,
pubmed-meshheading:12225959-RNA, Messenger,
pubmed-meshheading:12225959-Rats,
pubmed-meshheading:12225959-Reperfusion Injury,
pubmed-meshheading:12225959-Transcription, Genetic,
pubmed-meshheading:12225959-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2002
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pubmed:articleTitle |
Mitogen-activated protein kinases regulate HO-1 gene transcription after ischemia-reperfusion lung injury.
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pubmed:affiliation |
Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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