{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1363670321066944128.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1258/ebm.2012.012212"}},{"identifier":{"@type":"URI","@value":"http://journals.sagepub.com/doi/pdf/10.1258/ebm.2012.012212"}},{"identifier":{"@type":"URI","@value":"http://journals.sagepub.com/doi/full-xml/10.1258/ebm.2012.012212"}}],"dc:title":[{"@value":"Cross-talk between inflammation and angiotensin II: Studies based on direct transfection of cardiomyocytes with AT1R and AT2R cDNA"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p> Ischemic myocardium exhibits inflammation, local angiotensin II (Ang II) generation and up-regulation of LOX-1, a lectin-like ox-LDL receptor. To define the inter-active roles of Ang II and inflammation in furthering tissue injury, cultured HL-1 cardiomyocytes were treated with Ang II. Ang II treatment up-regulated the expression of Ang II type 1 (AT1R) and type 2 (AT2R) receptors as well as LOX-1. Ang II also activated p44/42MAPK, p38MAPK, c-Jun and NF-kB, and increased the expression of inflammation-related genes (interleukins-6, interleukins-10, tumor necrosis factor-a, intercellular adhesion molecule-1). To study how inflammation per se might affect expression of Ang II receptors and LOX-1, cultured, cardiomyocytes were treated with lipopolysaccharide (LPS). Like Ang II, LPS increased the expression of AT1R, AT2R and LOX-1. LPS also activated mitogen-acticated protein kinase (MAPKs), c-Jun and NF-kB, and pro-inflammatory genes. The selective inhibitors of MAPKs, c-Jun and NF-kB each blocked the transcription of LOX-1 and pro-inflammatory genes in response to Ang II as well as LPS. These observations suggested a positive feedback between Ang II and inflammation. To delineate the role of AT1R and AT2R in LOX-1 expression, another set of cardiomyocytes were transfected with AT1R or AT2R cDNA. Forced over-expression of AT1R resulted in activation of MAPKs, c-Jun and NF-kB, up-regulation of inflammatory genes and LOX-1; on the other hand forced AT2R over-expression induced up-regulation of pro-apoptotic signals (pro-IL-1b and IL-1b), and decreased LOX-1 expression. These studies show that both Ang II and inflammation mediator LPS up-regulate AT1R, AT2R and LOX-1 expression. Up-regulation of AT1R promotes inflammation and LOX-1 expression, whereas up-regulation of AT2R promotes apoptosis signals and decreases LOX-1 expression. </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1383670321066944133","@type":"Researcher","foaf:name":[{"@value":"Wang Xianwei"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670321066944130","@type":"Researcher","foaf:name":[{"@value":"Khaidakov Magomed"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670321066944131","@type":"Researcher","foaf:name":[{"@value":"Zufeng Ding"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670321066944134","@type":"Researcher","foaf:name":[{"@value":"Mitra Sona"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670321066944132","@type":"Researcher","foaf:name":[{"@value":"Lu Jingjun"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670321066944128","@type":"Researcher","foaf:name":[{"@value":"Liu Shijie"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670321066944129","@type":"Researcher","foaf:name":[{"@value":"Jawahar L Mehta"}],"jpcoar:affiliationName":[{"@value":"Central Arkansas Veterans Healthcare System, Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"15353702"},{"@type":"EISSN","@value":"15353699"}],"prism:publicationName":[{"@value":"Experimental Biology and Medicine"}],"dc:publisher":[{"@value":"Frontiers Media SA"}],"prism:publicationDate":"2012-12","prism:volume":"237","prism:number":"12","prism:startingPage":"1394","prism:endingPage":"1401"},"reviewed":"false","dc:rights":["http://journals.sagepub.com/page/policies/text-and-data-mining-license"],"url":[{"@id":"http://journals.sagepub.com/doi/pdf/10.1258/ebm.2012.012212"},{"@id":"http://journals.sagepub.com/doi/full-xml/10.1258/ebm.2012.012212"}],"createdAt":"2013-01-25","modifiedAt":"2025-04-07","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/2050588892097690880","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Olmesartan protects endothelial cells against oxidative stress-mediated cellular injury"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1258/ebm.2012.012212"},{"@type":"CROSSREF","@value":"10.1007/s10157-015-1111-5_references_DOI_QQzbNoywNUIm4BphJ4L5GAkSYky"}]}