{"created":"2023-07-27T06:39:05.099899+00:00","id":27393,"links":{},"metadata":{"_buckets":{"deposit":"bafdfeaf-9305-4521-97ac-2c49aa7da28e"},"_deposit":{"created_by":3,"id":"27393","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"27393"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00027393","sets":["1777:1778:1779"]},"author_link":["47562","47565","47563","47564","49"],"item_4_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2008-09-01","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"1622","bibliographicPageStart":"1614","bibliographicVolumeNumber":"14","bibliographic_titles":[{"bibliographic_title":"Molecular Vision"}]}]},"item_4_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Purpose: To evaluate the roles of CCL3 and its specific chemokine receptors, CCR1 and CCR5, in alkali-induced corneal neovascularization (CNV). Methods: Chemical denudation of corneal and limbal epithelium was performed on wild-type (WT) BALB/c mice and CCL3-, CCR1-, and CCR5-deficienct (knockout [KO]) counterparts. Two weeks after injury CNV was quantified by immunostaining with anti-CD31. Angiogenic factor expression and leukocyte accumulation in the early phase after injury were quantified by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemical analysis, respectively. Results: Alkali injury augmented the intraocular mRNA expression of CCL3 and its receptors, CCR1 and CCR5, together with a transient infiltration of F4/80 positive macrophages and Gr-1 positive neutrophils. Compared with WT mice, CCL3-KO and CCR5-KO mice but not CCR1-KO mice exhibited reduced CNV two weeks after injury both macroscopically and microscopically as evidenced by CD31 positive areas. Concomitantly, the infiltration of F4/80 positive macrophages but not Gr-1 positive neutrophils was significantly attenuated in CCL3-KO mice compared with WT mice. Intracorneal infiltration of CCR5 expressing cells was significantly impaired in CCL3-KO mice compared with WT mice. Alkali injury induced a massive increase in the intraocular mRNA expression of a potent angiogenic factor, vascular endothelial growth factor (VEGF), in WT mice whereas these increments were severely retarded in CCL3-KO mice. Moreover, CCL3 enhanced VEGF expression by murine peritoneal macrophages at both the mRNA and the protein level. Furthermore, topical CCL3 application restored CNV, which was macroscopically and microscopically reduced in CCL3-KO mice after two weeks to levels similar to those found in WT mice. Conclusions: In alkali-induced CNV, CCL3 induced macrophages to infiltrate and produce VEGF by binding to CCR5 but not to CCR1 and eventually promoted angiogenesis. © 2008 Molecular Vision.","subitem_description_type":"Abstract"}]},"item_4_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学がん研究所がん病態制御","subitem_description_type":"Other"}]},"item_4_publisher_17":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Molecular Vision"}]},"item_4_source_id_11":{"attribute_name":"NCID","attribute_value_mlt":[{"subitem_source_identifier":"AA12037116","subitem_source_identifier_type":"NCID"}]},"item_4_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"1090-0535","subitem_source_identifier_type":"ISSN"}]},"item_4_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Lu, Peirong"}],"nameIdentifiers":[{"nameIdentifier":"47562","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Li, Longbiao"}],"nameIdentifiers":[{"nameIdentifier":"47563","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Wu, Yu Ying"}],"nameIdentifiers":[{"nameIdentifier":"47564","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Mukaida, Naofumi"}],"nameIdentifiers":[{"nameIdentifier":"49","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"30182067","nameIdentifierScheme":"e-Rad","nameIdentifierURI":"https://kaken.nii.ac.jp/ja/search/?qm=30182067"},{"nameIdentifier":"30182067","nameIdentifierScheme":"金沢大学研究者情報","nameIdentifierURI":"http://ridb.kanazawa-u.ac.jp/public/detail.php?kaken=30182067"},{"nameIdentifier":"30182067","nameIdentifierScheme":"研究者番号","nameIdentifierURI":"https://nrid.nii.ac.jp/nrid/1000030182067"}]},{"creatorNames":[{"creatorName":"Zhang, Xueguang Guang"}],"nameIdentifiers":[{"nameIdentifier":"47565","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-10-05"}],"displaytype":"detail","filename":"CA-PR-MUKAIDA-N-1614.pdf","filesize":[{"value":"286.1 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"CA-PR-MUKAIDA-N-1614.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/27393/files/CA-PR-MUKAIDA-N-1614.pdf"},"version_id":"94fe48c3-5532-46e2-9f43-258f0d9cc074"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"Essential contribution of CCL3 to alkali-induced corneal neovascularization by regulating vascular endothelial growth factor production by macrophages","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Essential contribution of CCL3 to alkali-induced corneal neovascularization by regulating vascular endothelial growth factor production by macrophages"}]},"item_type_id":"4","owner":"3","path":["1779"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-10-05"},"publish_date":"2017-10-05","publish_status":"0","recid":"27393","relation_version_is_last":true,"title":["Essential contribution of CCL3 to alkali-induced corneal neovascularization by regulating vascular endothelial growth factor production by macrophages"],"weko_creator_id":"3","weko_shared_id":3},"updated":"2024-06-25T04:59:34.591462+00:00"}