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Article: Ischemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats
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TitleIschemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats
 
AuthorsWu, H4
Lei, S1
Yuan, J4
Liu, X3
Zhang, D4
Gu, X3
Zhang, L3
Xia, Z2 3
 
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
 
CitationJournal of Surgical Research, 2013, v. 181 n. 2, p. 204-212 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jss.2012.07.031
 
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.
 
ISSN0022-4804
2013 Impact Factor: 2.121
 
DOIhttp://dx.doi.org/10.1016/j.jss.2012.07.031
 
DC FieldValue
dc.contributor.authorWu, H
 
dc.contributor.authorLei, S
 
dc.contributor.authorYuan, J
 
dc.contributor.authorLiu, X
 
dc.contributor.authorZhang, D
 
dc.contributor.authorGu, X
 
dc.contributor.authorZhang, L
 
dc.contributor.authorXia, Z
 
dc.date.accessioned2012-09-20T07:50:52Z
 
dc.date.available2012-09-20T07:50:52Z
 
dc.date.issued2013
 
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.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationJournal of Surgical Research, 2013, v. 181 n. 2, p. 204-212 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.jss.2012.07.031
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.jss.2012.07.031
 
dc.identifier.hkuros209806
 
dc.identifier.issn0022-4804
2013 Impact Factor: 2.121
 
dc.identifier.pmid22878149
 
dc.identifier.scopuseid_2-s2.0-84876408681
 
dc.identifier.urihttp://hdl.handle.net/10722/163750
 
dc.languageeng
 
dc.publisherElsevier Inc.. The Journal's web site is located at http://www.elsevier.com/locate/jsre
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Surgical Research
 
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 rats
 
dc.typeArticle
 
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<item><contributor.author>Wu, H</contributor.author>
<contributor.author>Lei, S</contributor.author>
<contributor.author>Yuan, J</contributor.author>
<contributor.author>Liu, X</contributor.author>
<contributor.author>Zhang, D</contributor.author>
<contributor.author>Gu, X</contributor.author>
<contributor.author>Zhang, L</contributor.author>
<contributor.author>Xia, Z</contributor.author>
<date.accessioned>2012-09-20T07:50:52Z</date.accessioned>
<date.available>2012-09-20T07:50:52Z</date.available>
<date.issued>2013</date.issued>
<identifier.citation>Journal of Surgical Research, 2013, v. 181 n. 2, p. 204-212</identifier.citation>
<identifier.issn>0022-4804</identifier.issn>
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<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.</description.abstract>
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<subject>Egr-1</subject>
<subject>Heme oxygenase 1</subject>
<subject>Ischemic postconditioning</subject>
<subject>Lung ischemia reperfusion</subject>
<title>Ischemic postconditioning downregulates Egr-1 expression and attenuates postischemic pulmonary inflammatory cytokine release and tissue injury in rats</title>
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Author Affiliations
  1. Hubei General Hospital
  2. The University of Hong Kong
  3. Guangdong Medical College
  4. Zunyi Medical College