Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 김태형 | - |
dc.date.accessioned | 2018-03-01T01:57:40Z | - |
dc.date.available | 2018-03-01T01:57:40Z | - |
dc.date.issued | 2012-09 | - |
dc.identifier.citation | American Journal of Respiratory Cell and Molecular Biology, Sep 2012, 47(3), P.372-378 | en_US |
dc.identifier.issn | 1044-1549 | - |
dc.identifier.uri | https://www.atsjournals.org/doi/abs/10.1165/rcmb.2012-0085OC | - |
dc.description.abstract | Insulin-like growth factor (IGF)-1 is increased in different models of acute lung injury, and is an important determinant of survival and proliferation in many cells. We previously demonstrated that treatment of mice with IGF-1 receptor-blocking antibody (A12) improved early survival in bleomycin-induced lung injury. We have now examined whether administration of A12 improved markers of lung injury in hyperoxia model of lung injury. C57BL/6 mice underwent intraperitoneal administration of A12 or control antibody (keyhole limpet hemocyanin [KLH]), then were exposed to 95% hyperoxia for 88-90 hours. Mice were killed and bronchoalveolar lavage (BAL) and lung tissue were obtained for analysis. Hyperoxia caused a significant increase in IGF levels in BAL and lung lysates. Peripheral blood neutrophils expressed IGF-1R at baseline and after hyperoxia. BAL neutrophils from hyperoxia-treated mice and patients with acute lung injury also expressed cell surface IGF-1R. A12-treated mice had significantly decreased polymorphonuclear cell (PMN) count in BAL compared with KLH control mice (P = 0.02). BAL from A12-treated mice demonstrated decreased PMN chemotactic activity compared with BAL from KLH-treated mice. Pretreatment of PMNs with A12 decreased their chemotactic response to BAL from hyperoxia exposed mice. Furthermore, IGF-1 induced a dose-dependent chemotaxis of PMNs. There were no differences in other chemotactic cytokines in BAL, including CXCL1 and CXCL2. In summary, IGF blockade decreased PMN recruitment to the alveolar space in a mouse model of hyperoxia. Furthermore, the decrease in BAL PMNs was at least partially due to a direct effect of A12 on PMN chemotaxis. | en_US |
dc.description.sponsorship | This work was supported by an American Heart Association Grant-in-Aid, by National Institutes of Health grants HL083481 and K24HL068796 (L.M.S.), and by a Parker B. Francis Fellowship (S.E.G.). | en_US |
dc.language.iso | en | en_US |
dc.publisher | Amer Thoracic SOC | en_US |
dc.subject | insulin-like growth factor | en_US |
dc.subject | hyperoxia-induced lung injury | en_US |
dc.subject | neutrophils | en_US |
dc.title | Effect of Insulin-Like Growth Factor Blockade on Hyperoxia-Induced Lung Injury | en_US |
dc.type | Article | en_US |
dc.relation.no | 3 | - |
dc.relation.volume | 47 | - |
dc.identifier.doi | 10.1165/rcmb.2012-0085OC | - |
dc.relation.page | 372-378 | - |
dc.relation.journal | AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY | - |
dc.contributor.googleauthor | Kim, Tae-Hyung | - |
dc.contributor.googleauthor | Chow, Yu-Hua | - |
dc.contributor.googleauthor | Gill, Sean E. | - |
dc.contributor.googleauthor | Schnapp, Lynn M. | - |
dc.contributor.googleauthor | 김태형 | - |
dc.contributor.googleauthor | 추유화 | - |
dc.relation.code | 2012200531 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | drterry | - |
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