| pubmed-article:10194478 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C0001554 | lld:lifeskim |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C0273115 | lld:lifeskim |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C0538674 | lld:lifeskim |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C1517499 | lld:lifeskim |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C1999230 | lld:lifeskim |
| pubmed-article:10194478 | lifeskim:mentions | umls-concept:C0205228 | lld:lifeskim |
| pubmed-article:10194478 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10194478 | pubmed:dateCreated | 1999-4-29 | lld:pubmed |
| pubmed-article:10194478 | pubmed:abstractText | Heme oxygenase-1 (HO-1) confers protection against a variety of oxidant-induced cell and tissue injury. In this study, we examined whether exogenous administration of HO-1 by gene transfer could also confer protection. We first demonstrated the feasibility of overexpressing HO-1 in the lung by gene transfer. A fragment of the rat HO-1 cDNA clone containing the entire coding region was cloned into plasmid pAC-CMVpLpA, and recombinant adenoviruses containing the rat HO-1 cDNA fragment Ad5-HO-1 were generated by homologous recombination. Intratracheal administration of Ad5-HO-1 resulted in a time-dependent increase in expression of HO-1 mRNA and protein in the rat lungs. Increased HO-1 protein expression was detected diffusely in the bronchiolar epithelium of rats receiving Ad5-HO-1, as assessed by immunohistochemical studies. We then examined whether ectopic expression of HO-1 could confer protection against hyperoxia-induced lung injury. Rats receiving Ad5-HO-1, but not AdV-betaGal, a recombinant adenovirus expressing Escherichia coli beta-galactosidase, before exposure to hyperoxia (>99% O2) exhibited marked reduction in lung injury, as assessed by volume of pleural effusion and histological analyses (significant reduction of edema, hemorrhage, and inflammation). In addition, rats receiving Ad5-HO-1 also exhibited increased survivability against hyperoxic stress when compared with rats receiving AdV-betaGal. Expression of the antioxidant enzymes manganese superoxide dismutase (Mn-SOD) and copper-zinc superoxide dismutase (CuZn-SOD) and of L-ferritin and H-ferritin was not affected by Ad5-HO-1 administration. Furthermore, rats treated with Ad5-HO-1 exhibited attenuation of hyperoxia-induced neutrophil inflammation and apoptosis. Taken together, these data suggest the feasibility of high-level HO-1 expression in the rat lung by gene delivery. To our knowledge, we have demonstrated for the first time that HO-1 can provide protection against hyperoxia-induced lung injury in vivo by modulation of neutrophil inflammation and lung apoptosis. | lld:pubmed |
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| pubmed-article:10194478 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10194478 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10194478 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10194478 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10194478 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10194478 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:10194478 | pubmed:author | pubmed-author:AlamJJ | lld:pubmed |
| pubmed-article:10194478 | pubmed:author | pubmed-author:CookJ LJL | lld:pubmed |
| pubmed-article:10194478 | pubmed:author | pubmed-author:KollsJ KJK | lld:pubmed |
| pubmed-article:10194478 | pubmed:author | pubmed-author:EhleMM | lld:pubmed |
| pubmed-article:10194478 | pubmed:author | pubmed-author:MantellL LLL | lld:pubmed |
| pubmed-article:10194478 | pubmed:author | pubmed-author:OtterbeinL... | lld:pubmed |
| pubmed-article:10194478 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10194478 | pubmed:volume | 103 | lld:pubmed |
| pubmed-article:10194478 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10194478 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10194478 | pubmed:pagination | 1047-54 | lld:pubmed |
| pubmed-article:10194478 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10194478 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10194478 | pubmed:articleTitle | Exogenous administration of heme oxygenase-1 by gene transfer provides protection against hyperoxia-induced lung injury. | lld:pubmed |
| pubmed-article:10194478 | pubmed:affiliation | Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06250, USA. | lld:pubmed |
| pubmed-article:10194478 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10194478 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10194478 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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