{"@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/1362825896000142592.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1089/ars.2005.7.1261"}},{"identifier":{"@type":"URI","@value":"http://www.liebertpub.com/doi/pdf/10.1089/ars.2005.7.1261"}},{"identifier":{"@type":"PMID","@value":"16115031"}},{"identifier":{"@type":"NAID","@value":"30018296032"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Reactive Oxygen Species-Mediated Signaling Pathways in Angiotensin II-Induced MCP- Expression of Proximal Tubular Cells"}],"description":[{"notation":[{"@value":"Angiotensin II (AngII) has pleiotropic effects, the most well known of which is the generation of reactive oxygen species (ROS) and chemokines in inflammatory lesions. Monocyte chemoattractant protein-1 (MCP-1) is considered a major chemokine in the pathogenesis of kidney diseases. We examined signaling pathways of AngII-induced MCP-1 expression and the role of ROS in the murine proximal tubular cells (mProx) using various inhibitors. Furthermore, we compared the signaling pathways between mProx and mesangial cells (MC). AngII-induced MCP-1 protein expression in mProx at 6 h was largely blocked by ROS (N-acetylcysteine; 82 +/- 14%), Ras (N-acetyl-S-trans,trans-farnesyl-L-cysteine; 82 +/- 13%), and nuclear factor-kappaB (NF-kappaB) (parthenolide; 89 +/- 7.9%) inhibitors. Both AT1 receptor (AT1R) (Olmesartan; 41 +/- 12%) and the AT2R (PD123319; 24 +/- 11%) antagonists partially blocked the MCP-1 expression. Furthermore, mitogen-activated protein kinase (MAPK) pathways were also implicated in this protein expression, but it is less dependent on ROS/Ras pathways. In MC, protein kinase (calphostin C; 84 +/- 2.8%) and NF-kappaB (89 +/- 1.4%) inhibitors attenuated acute AngII-induced MCP-1 expression stronger than ROS/Ras inhibitors (1.0 +/- 0.9/29 +/- 9.5%). MAPK pathways, especially p38 MAPK, were involved in MC more than in mProx. AT1R (69 +/- 8.6%) and AT2R (57 +/- 21%) antagonists also were blocked. We suggested that, although NF-kappaB activation has a critical role, signaling pathways are different between mProx and MC. ROS-mediated signaling in mProx may have more contribution to AngII-induced inflammatory responses than to those in MC."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825896000142597","@type":"Researcher","foaf:name":[{"@value":"Chiaki Tanifuji"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142596","@type":"Researcher","foaf:name":[{"@value":"Yusuke Suzuki"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142593","@type":"Researcher","foaf:name":[{"@value":"Wong Mu Geot"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan."},{"@value":"Renal Unit, Department of Medicine, University Malaya Medical Center, Kuala Lumpur, Malaysia."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142599","@type":"Researcher","foaf:name":[{"@value":"Satoshi Horikoshi"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142594","@type":"Researcher","foaf:name":[{"@value":"Takeshi Sugaya"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142598","@type":"Researcher","foaf:name":[{"@value":"Marta Ruiz-Ortega"}],"jpcoar:affiliationName":[{"@value":"Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142595","@type":"Researcher","foaf:name":[{"@value":"Jesus Egido"}],"jpcoar:affiliationName":[{"@value":"Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain."}]},{"@id":"https://cir.nii.ac.jp/crid/1382825896000142592","@type":"Researcher","foaf:name":[{"@value":"Andyasuhiko Tomino"}],"jpcoar:affiliationName":[{"@value":"Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"15230864"},{"@type":"EISSN","@value":"15577716"}],"prism:publicationName":[{"@value":"Antioxidants & Redox Signaling"}],"dc:publisher":[{"@value":"SAGE Publications"}],"prism:publicationDate":"2005-09","prism:volume":"7","prism:number":"9-10","prism:startingPage":"1261","prism:endingPage":"1268"},"reviewed":"false","url":[{"@id":"http://www.liebertpub.com/doi/pdf/10.1089/ars.2005.7.1261"}],"createdAt":"2005-08-22","modifiedAt":"2026-02-18","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Time%20Factors","dc:title":"Time Factors"},{"@id":"https://cir.nii.ac.jp/all?q=Pyridines","dc:title":"Pyridines"},{"@id":"https://cir.nii.ac.jp/all?q=Blotting,%20Western","dc:title":"Blotting, Western"},{"@id":"https://cir.nii.ac.jp/all?q=Tetrazoles","dc:title":"Tetrazoles"},{"@id":"https://cir.nii.ac.jp/all?q=Enzyme-Linked%20Immunosorbent%20Assay","dc:title":"Enzyme-Linked Immunosorbent Assay"},{"@id":"https://cir.nii.ac.jp/all?q=Angiotensin%20II%20Type%202%20Receptor%20Blockers","dc:title":"Angiotensin II Type 2 Receptor 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