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Exogenous administration of heme oxygenase-1 by gene transfer provides protection against hyperoxia-induced lung injury
Open accessAbstract
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.
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Choi, A. M., & Alam, J. (1996) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/ajrcmb.15.1.8679227 · Cited by 1,126
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Metadata
- Authors
- Otterbein, L. E., Kolls, J. K., Mantell, L. L., Cook, J. L., Alam, J., & Choi, A. M. K.
- Venue
- Journal of Clinical Investigation
- Published
- 1999-04-01
- Volume
- 103
- Issue
- 7
- Pages
- 1047-1054
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2145287139
- Cited by
- 492
- References
- 1
- FWCI
- 13.38
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Otterbein, L. E., Kolls, J. K., Mantell, L. L., Cook, J. L., Alam, J., & Choi, A. M. K. (1999). Exogenous administration of heme oxygenase-1 by gene transfer provides protection against hyperoxia-induced lung injury. Journal of Clinical Investigation. https://doi.org/10.1172/jci5342
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