{"_buckets": {"deposit": "ac6d40ab-04e5-406c-96e0-1c6cf301fc55"}, "_deposit": {"id": "20089", "owners": [], "pid": {"revision_id": 0, "type": "depid", "value": "20089"}, "status": "published"}, "_oai": {"id": "oai:soar-ir.repo.nii.ac.jp:00020089"}, "item_6_biblio_info_6": {"attribute_name": "\u66f8\u8a8c\u60c5\u5831", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2013-08-08", "bibliographicIssueDateType": "Issued"}, "bibliographicIssueNumber": "8", "bibliographicPageStart": "e70533", "bibliographicVolumeNumber": "8", "bibliographic_titles": [{"bibliographic_title": "PLOS ONE"}]}]}, "item_6_description_20": {"attribute_name": "\u6284\u9332", "attribute_value_mlt": [{"subitem_description": "Objectives\nIncreased plasma C-reactive protein (CRP) levels are associated with the occurrence and severity of acute coronary syndrome. We investigated whether CRP can be generated in vascular endothelial cells (ECs) after exposure to the most electronegative subfraction of low-density lipoprotein (LDL), L5, which is atherogenic to ECs. Because L5 and CRP are both ligands for the lectin-like oxidized LDL receptor-1 (LOX-1), we also examined the role of LOX-1.\nMethods and Results\nPlasma LDL samples isolated from asymptomatic hypercholesterolemic (LDL cholesterol [LDL-C] levels, 154.6\u00b120 mg/dL; n\u200a=\u200a7) patients and normocholesterolemic (LDL-C levels, 86.1\u00b121 mg/dL; P\u003c0.001; n\u200a=\u200a7) control individuals were chromatographically resolved into 5 subfractions, L1-L5. The L5 percentage (L5%) and the plasma L5 concentration ([L5] \u200a=\u200a L5% \u00d7 LDL-C) in the patient and control groups were 8.1\u00b12% vs. 2.3\u00b11% (P\u003c0.001) and 12.6\u00b14 mg/dL vs. 1.9\u00b11 mg/dL (P\u003c0.001), respectively. In hypercholesterolemic patients treated with atorvastatin for 6 months (10 mg/day), [L5] decreased from 12.6\u00b14 mg/dL to 4.5\u00b11.1 mg/dL (P\u200a=\u200a0.011; n\u200a=\u200a5), whereas both [L5] and L5% returned to baseline levels in 2 noncompliant patients 3 months after discontinuation. In cultured human aortic ECs (HAECs), L5 upregulated CRP expression in a dose- and time-dependent manner up to 2.5-fold (P\u003c0.01), whereas the least electronegative subfraction, L1, had no effect. DiI-labeled L1, internalized through the LDL receptor, became visible inside HAECs within 30 seconds. In contrast, DiI-labeled L5, internalized through LOX-1, became apparent after 5 minutes. L5-induced CRP expression manifested at 30 minutes and was attenuated by neutralizing LOX-1. After 30 minutes, L5 but not L1 induced reactive oxygen species (ROS) production. Both L5-induced ROS and CRP production were attenuated by ROS inhibitor N-acetyl cysteine.\nConclusions\nOur results suggest that CRP, L5, and LOX-1 form a cyclic mechanism in atherogenesis and that reducing plasma L5 levels with atorvastatin disrupts the vascular toxicity of L5.", "subitem_description_type": "Abstract"}]}, "item_6_description_30": {"attribute_name": "\u8cc7\u6e90\u30bf\u30a4\u30d7\uff08\u30b3\u30f3\u30c6\u30f3\u30c4\u306e\u7a2e\u985e\uff09", "attribute_value_mlt": [{"subitem_description": "Article", "subitem_description_type": "Other"}]}, "item_6_description_5": {"attribute_name": "\u5f15\u7528", "attribute_value_mlt": [{"subitem_description": "PLOS ONE.8(8):e70533(2013)", "subitem_description_type": "Other"}]}, "item_6_link_3": {"attribute_name": "\u4fe1\u5dde\u5927\u5b66\u7814\u7a76\u8005\u7dcf\u89a7\u3078\u306e\u30ea\u30f3\u30af", "attribute_value_mlt": [{"subitem_link_text": "Sawamura, Tatsuya", "subitem_link_url": "http://soar-rd.shinshu-u.ac.jp/profile/ja.HafpjeAF.html"}]}, "item_6_link_67": {"attribute_name": "WoS", "attribute_value_mlt": [{"subitem_link_text": "Web of Science", "subitem_link_url": "http://gateway.isiknowledge.com/gateway/Gateway.cgi?\u0026GWVersion=8\u0026SrcAuth=ShinshuUniv\u0026SrcApp=ShinshuUniv\u0026DestLinkType=FullRecord\u0026DestApp=WOS\u0026KeyUT=000323124000020"}]}, "item_6_publisher_4": {"attribute_name": "\u51fa\u7248\u8005", "attribute_value_mlt": [{"subitem_publisher": "PUBLIC LIBRARY SCIENCE"}]}, "item_6_relation_47": {"attribute_name": "PubMed", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "23950953"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://www.ncbi.nlm.nih.gov/pubmed/23950953", "subitem_relation_type_select": "PMID"}}]}, "item_6_relation_48": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "10.1371/journal.pone.0070533"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://doi.org/10.1371/journal.pone.0070533", "subitem_relation_type_select": "DOI"}}]}, "item_6_rights_62": {"attribute_name": "\u6a29\u5229", "attribute_value_mlt": [{"subitem_rights": "\u00a9 2013 Chu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited."}]}, "item_6_select_64": {"attribute_name": "\u8457\u8005\u7248\u30d5\u30e9\u30b0", "attribute_value_mlt": [{"subitem_select_item": "publisher"}]}, "item_6_source_id_35": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "1932-6203", "subitem_source_identifier_type": "ISSN"}]}, "item_6_source_id_39": {"attribute_name": "NII ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "1932-6203", "subitem_source_identifier_type": "ISSN"}]}, "item_6_text_70": {"attribute_name": "wosonly keywords", "attribute_value_mlt": [{"subitem_text_value": "ACUTE CORONARY SYNDROMES; FIBROBLAST-GROWTH-FACTOR; STATIN THERAPY; LECTIN-LIKE; ATHEROSCLEROSIS; DISEASE; PREVENTION; RISK; INFLAMMATION; CHOLESTEROL"}]}, "item_6_textarea_68": {"attribute_name": "wosonly abstract", "attribute_value_mlt": [{"subitem_textarea_value": "Objectives: Increased plasma C-reactive protein (CRP) levels are associated with the occurrence and severity of acute coronary syndrome. We investigated whether CRP can be generated in vascular endothelial cells (ECs) after exposure to the most electronegative subfraction of low-density lipoprotein (LDL), L5, which is atherogenic to ECs. Because L5 and CRP are both ligands for the lectin-like oxidized LDL receptor-1 (LOX-1), we also examined the role of LOX-1. \nMethods and Results: Plasma LDL samples isolated from asymptomatic hypercholesterolemic (LDL cholesterol [LDL-C] levels, 154.6 +/- 20 mg/dL; n = 7) patients and normocholesterolemic (LDL-C levels, 86.1 +/- 21 mg/dL; P \u003c 0.001; n = 7) control individuals were chromatographically resolved into 5 subfractions, L1-L5. The L5 percentage (L5%) and the plasma L5 concentration ([L5] = L5% x LDL-C) in the patient and control groups were 8.1 +/- 2% vs. 2.3 +/- 1% (P\u003c0.001) and 12.6 +/- 4 mg/dL vs. 1.9 +/- 1 mg/dL (P\u003c0.001), respectively. In hypercholesterolemic patients treated with atorvastatin for 6 months (10 mg/day), [L5] decreased from 12.664 mg/dL to 4.561.1 mg/dL (P = 0.011; n = 5), whereas both [L5] and L5% returned to baseline levels in 2 noncompliant patients 3 months after discontinuation. In cultured human aortic ECs (HAECs), L5 upregulated CRP expression in a dose- and time-dependent manner up to 2.5-fold (P \u003c 0.01), whereas the least electronegative subfraction, L1, had no effect. DiI-labeled L1, internalized through the LDL receptor, became visible inside HAECs within 30 seconds. In contrast, DiI-labeled L5, internalized through LOX-1, became apparent after 5 minutes. L5-induced CRP expression manifested at 30 minutes and was attenuated by neutralizing LOX-1. After 30 minutes, L5 but not L1 induced reactive oxygen species (ROS) production. Both L5-induced ROS and CRP production were attenuated by ROS inhibitor N-acetyl cysteine. \nConclusions: Our results suggest that CRP, L5, and LOX-1 form a cyclic mechanism in atherogenesis and that reducing plasma L5 levels with atorvastatin disrupts the vascular toxicity of L5."}]}, "item_creator": {"attribute_name": "\u8457\u8005", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Chu, CS"}], "nameIdentifiers": [{"nameIdentifier": "106234", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Wang, YC"}], "nameIdentifiers": [{"nameIdentifier": "106235", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Lu, LS"}], "nameIdentifiers": [{"nameIdentifier": "106236", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Walton, B"}], "nameIdentifiers": [{"nameIdentifier": "106237", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Yilmaz, HR"}], "nameIdentifiers": [{"nameIdentifier": "106238", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Huang, RY"}], "nameIdentifiers": [{"nameIdentifier": "106239", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Sawamura, T"}], "nameIdentifiers": [{"nameIdentifier": "106240", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Dixon, RAF"}], "nameIdentifiers": [{"nameIdentifier": "106241", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Lai, WT"}], "nameIdentifiers": [{"nameIdentifier": "106242", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Chen, CH"}], "nameIdentifiers": [{"nameIdentifier": "106243", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Lu, J"}], "nameIdentifiers": [{"nameIdentifier": "106244", "nameIdentifierScheme": "WEKO"}]}]}, "item_files": {"attribute_name": "\u30d5\u30a1\u30a4\u30eb\u60c5\u5831", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2018-09-12"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "25293063_20.pdf", "filesize": [{"value": "3.9 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensefree": "\u00a9 2013 Chu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.", "licensetype": "license_free", "mimetype": "application/pdf", "size": 3900000.0, "url": {"label": "25293063_20.pdf", "url": "https://soar-ir.repo.nii.ac.jp/record/20089/files/25293063_20.pdf"}, "version_id": "cbdf0b85-b3c3-4d99-831c-fef2d177a8ed"}]}, "item_language": {"attribute_name": "\u8a00\u8a9e", "attribute_value_mlt": [{"subitem_language": "eng"}]}, "item_resource_type": {"attribute_name": "\u8cc7\u6e90\u30bf\u30a4\u30d7", "attribute_value_mlt": [{"resourcetype": "journal article", "resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_title": "Electronegative Low-Density Lipoprotein Increases C-Reactive Protein Expression in Vascular Endothelial Cells through the LOX-1 Receptor", "item_titles": {"attribute_name": "\u30bf\u30a4\u30c8\u30eb", "attribute_value_mlt": [{"subitem_title": "Electronegative Low-Density Lipoprotein Increases C-Reactive Protein Expression in Vascular Endothelial Cells through the LOX-1 Receptor"}]}, "item_type_id": "6", "owner": "1", "path": ["461/462"], "permalink_uri": "http://hdl.handle.net/10091/00020850", "pubdate": {"attribute_name": "\u516c\u958b\u65e5", "attribute_name_i18n": "\u516c\u958b\u65e5", "attribute_value": "2018-09-12"}, "publish_date": "2018-09-12", "publish_status": "0", "recid": "20089", "relation": {}, "relation_version_is_last": true, "title": ["Electronegative Low-Density Lipoprotein Increases C-Reactive Protein Expression in Vascular Endothelial Cells through the LOX-1 Receptor"], "weko_shared_id": null}