2001
DOI: 10.1038/sj.gt.3301540
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Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

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Cited by 135 publications
(104 citation statements)
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References 59 publications
(70 reference statements)
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“…Interestingly, the upregulation of stress proteins such as HO-1 and Hsp70 has been shown to limit inflammatory responses in many models [148][149][150]. Moreover, CO treatment in vivo has been shown to induce HO-1 in the liver [129] and Hsp70 in the lung [130].…”
Section: Co Signalingmentioning
confidence: 99%
“…Interestingly, the upregulation of stress proteins such as HO-1 and Hsp70 has been shown to limit inflammatory responses in many models [148][149][150]. Moreover, CO treatment in vivo has been shown to induce HO-1 in the liver [129] and Hsp70 in the lung [130].…”
Section: Co Signalingmentioning
confidence: 99%
“…These cytoprotective functions can be applied for therapeutic purposes. We previously reported that chemical induction of HO-1 suppresses lupus nephritis (15) and that adenovirus vector-mediated gene transfer of HO-1 complementary DNA (cDNA) has beneficial effects on lipopolysaccharide (LPS)-induced lung injury (16), influenza viral pneumonia (17), bleomycin-induced pulmonary fibrosis (18), Pseudomonas chronic respiratory infection (19), and elastase-induced emphysema (20) in mouse models. Similarly, favorable outcomes have been achieved with therapies using HO-1 chemical inducers or with gene transfer in other animal models, including ischemia/ reperfusion-induced injuries of the heart (9) and liver (21), LPS-induced ocular inflammation (22), and allogenic heart allotransplantation (23).…”
mentioning
confidence: 99%
“…10 Of particular interest is a study demonstrating that adenovirus-mediated transfer of heme oxygenase-1 (HO-1) cDNA reduces the lung damage and influx of leukocytes in influenzainfected mice, while markedly boosting survival (60% vs. 0% in controls). 33 HO-1 generates bilirubin, which recently has been shown to be a potent physiological inhibitor of NADPH oxidase activity. [34][35][36][37] The possibility that concurrent generation of carbon monoxide also contributed to the observed protection merits consideration, but it is reasonable to suspect that the potent antioxidant activity of bilirubin contributed prominently to the protection afforded by HO-1 transfection.…”
Section: Nadph Oxidase As a Potential Targetmentioning
confidence: 99%