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- Publisher Website: 10.1016/j.jss.2012.07.031
- Scopus: eid_2-s2.0-84876408681
- PMID: 22878149
- WOS: WOS:000317742800010
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Article: Ischemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats
Title | Ischemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats |
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Authors | |
Keywords | Egr-1 Heme oxygenase 1 Ischemic postconditioning Lung ischemia reperfusion |
Issue Date | 2013 |
Publisher | Elsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsre |
Citation | Journal of Surgical Research, 2013, v. 181 n. 2, p. 204-212 How to Cite? |
Abstract | BACKGROUND: The early growth response-1 (Egr-1) gene is upregulated after an ischemia-reperfusion (IR) challenge and upregulates target genes, such as proinflammatory cytokines. Ischemic postconditioning (IPostC) attenuates lung IR injury and reduces the systemic inflammatory response by activating heme oxygenase-1 (HO-1). However, the role of Egr-1 in IPostC protection against lung IR injury and inflammation and its interplay with HO-1 in IPostC protection is unknown. MATERIALS AND METHODS: Sprague-Dawley rats or cultured A549 cells were subjected to IR or hypoxia/reoxygenation with or without IPostC or hypoxic postconditioning in the presence or absence of Egr-1 inhibition using Egr-1 antisense oligodeoxyrinonucleotide or Egr-1 small interfering RNA transfection. Lung injury was assessed by measuring the lung wet/dry weight ratio, histologic change, and malondialdehyde content. The amount of lactate dehydrogenase release in culture medium was detected to evaluate cell injury. The protein expression of Egr-1, interleukin (IL)-1beta, and HO-1 was assessed by Western blot. RESULTS: Inhibition of Egr-1 significantly attenuated lung IR injury and the inflammation response caused by IR or hypoxia/reoxygenation, as shown by the alleviated lung pathologic changes, decreased pulmonary malondialdehyde content, wet/dry ratio, reduced release of the cytokines tumor necrosis factor-alpha, IL-6, and IL-8 in the bronchoalveolar lavage, and reduced Egr-1, IL-1beta, and HO-1 protein expression and HO-1 activity. IPostC or hypoxic postconditioning reduced the postischemic Egr-1 expression and conferred similar protection against lung IR injury as Egr-1 inhibition. CONCLUSIONS: Egr-1 plays an important role in regulating the HO-1 production induced by IR or hypoxia/reoxygenation. Thus, downregulation of Egr-1 expression might represent one of the major mechanisms whereby IPostC confers protection against pulmonary IR insult. |
Persistent Identifier | http://hdl.handle.net/10722/163750 |
ISSN | 2023 Impact Factor: 1.8 2023 SCImago Journal Rankings: 0.748 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wu, H | en_US |
dc.contributor.author | Lei, S | en_US |
dc.contributor.author | Yuan, J | en_US |
dc.contributor.author | Liu, X | en_US |
dc.contributor.author | Zhang, D | en_US |
dc.contributor.author | Gu, X | en_US |
dc.contributor.author | Zhang, L | en_US |
dc.contributor.author | Xia, Z | en_US |
dc.date.accessioned | 2012-09-20T07:50:52Z | - |
dc.date.available | 2012-09-20T07:50:52Z | - |
dc.date.issued | 2013 | en_US |
dc.identifier.citation | Journal of Surgical Research, 2013, v. 181 n. 2, p. 204-212 | en_US |
dc.identifier.issn | 0022-4804 | - |
dc.identifier.uri | http://hdl.handle.net/10722/163750 | - |
dc.description.abstract | BACKGROUND: The early growth response-1 (Egr-1) gene is upregulated after an ischemia-reperfusion (IR) challenge and upregulates target genes, such as proinflammatory cytokines. Ischemic postconditioning (IPostC) attenuates lung IR injury and reduces the systemic inflammatory response by activating heme oxygenase-1 (HO-1). However, the role of Egr-1 in IPostC protection against lung IR injury and inflammation and its interplay with HO-1 in IPostC protection is unknown. MATERIALS AND METHODS: Sprague-Dawley rats or cultured A549 cells were subjected to IR or hypoxia/reoxygenation with or without IPostC or hypoxic postconditioning in the presence or absence of Egr-1 inhibition using Egr-1 antisense oligodeoxyrinonucleotide or Egr-1 small interfering RNA transfection. Lung injury was assessed by measuring the lung wet/dry weight ratio, histologic change, and malondialdehyde content. The amount of lactate dehydrogenase release in culture medium was detected to evaluate cell injury. The protein expression of Egr-1, interleukin (IL)-1beta, and HO-1 was assessed by Western blot. RESULTS: Inhibition of Egr-1 significantly attenuated lung IR injury and the inflammation response caused by IR or hypoxia/reoxygenation, as shown by the alleviated lung pathologic changes, decreased pulmonary malondialdehyde content, wet/dry ratio, reduced release of the cytokines tumor necrosis factor-alpha, IL-6, and IL-8 in the bronchoalveolar lavage, and reduced Egr-1, IL-1beta, and HO-1 protein expression and HO-1 activity. IPostC or hypoxic postconditioning reduced the postischemic Egr-1 expression and conferred similar protection against lung IR injury as Egr-1 inhibition. CONCLUSIONS: Egr-1 plays an important role in regulating the HO-1 production induced by IR or hypoxia/reoxygenation. Thus, downregulation of Egr-1 expression might represent one of the major mechanisms whereby IPostC confers protection against pulmonary IR insult. | - |
dc.language | eng | en_US |
dc.publisher | Elsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsre | - |
dc.relation.ispartof | Journal of Surgical Research | en_US |
dc.subject | Egr-1 | - |
dc.subject | Heme oxygenase 1 | - |
dc.subject | Ischemic postconditioning | - |
dc.subject | Lung ischemia reperfusion | - |
dc.title | Ischemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats | en_US |
dc.type | Article | en_US |
dc.identifier.email | Zhang, L: zhanglq1970@163.com | en_US |
dc.identifier.email | Xia, Z: zyxia@hku.hk | - |
dc.identifier.authority | Xia, Z=rp00532 | en_US |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.jss.2012.07.031 | - |
dc.identifier.pmid | 22878149 | - |
dc.identifier.scopus | eid_2-s2.0-84876408681 | - |
dc.identifier.hkuros | 209806 | en_US |
dc.identifier.isi | WOS:000317742800010 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0022-4804 | - |