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Article: Ischemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats

TitleIschemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats
Authors
KeywordsEgr-1
Heme oxygenase 1
Ischemic postconditioning
Lung ischemia reperfusion
Issue Date2013
PublisherElsevier 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 Identifierhttp://hdl.handle.net/10722/163750
ISSN
2013 Impact Factor: 2.121
ISI Accession Number ID

 

Author Affiliations
  1. Hubei General Hospital
  2. The University of Hong Kong
  3. Guangdong Medical College
  4. Zunyi Medical College
DC FieldValueLanguage
dc.contributor.authorWu, Hen_US
dc.contributor.authorLei, Sen_US
dc.contributor.authorYuan, Jen_US
dc.contributor.authorLiu, Xen_US
dc.contributor.authorZhang, Den_US
dc.contributor.authorGu, Xen_US
dc.contributor.authorZhang, Len_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-09-20T07:50:52Z-
dc.date.available2012-09-20T07:50:52Z-
dc.date.issued2013en_US
dc.identifier.citationJournal of Surgical Research, 2013, v. 181 n. 2, p. 204-212en_US
dc.identifier.issn0022-4804-
dc.identifier.urihttp://hdl.handle.net/10722/163750-
dc.description.abstractBACKGROUND: 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.languageengen_US
dc.publisherElsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsre-
dc.relation.ispartofJournal of Surgical Researchen_US
dc.subjectEgr-1-
dc.subjectHeme oxygenase 1-
dc.subjectIschemic postconditioning-
dc.subjectLung ischemia reperfusion-
dc.titleIschemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in ratsen_US
dc.typeArticleen_US
dc.identifier.emailZhang, L: zhanglq1970@163.comen_US
dc.identifier.emailXia, Z: zyxia@hku.hk-
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jss.2012.07.031-
dc.identifier.pmid22878149-
dc.identifier.scopuseid_2-s2.0-84876408681-
dc.identifier.hkuros209806en_US
dc.identifier.isiWOS:000317742800010-
dc.publisher.placeUnited States-

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