{"created":"2023-05-15T16:43:01.279505+00:00","id":18202,"links":{},"metadata":{"_buckets":{"deposit":"7f30fea5-421b-481a-b265-68092e47ebd6"},"_deposit":{"created_by":2,"id":"18202","owners":[2],"pid":{"revision_id":0,"type":"depid","value":"18202"},"status":"published"},"_oai":{"id":"oai:nagasaki-u.repo.nii.ac.jp:00018202","sets":["73:74"]},"author_link":["72540","72539","72541","72538","72542"],"item_2_biblio_info_6":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2008-02-08","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"6","bibliographicPageEnd":"5","bibliographicPageStart":"1","bibliographicVolumeNumber":"4","bibliographic_titles":[{"bibliographic_title":"Molecular Pain"}]}]},"item_2_description_4":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Recently, we reported that lysophosphatidic acid (LPA) induces long-lasting mechanical allodynia and thermal hyperalgesia as well as demyelination and upregulation of pain-related proteins through one of its cognate receptors, LPA1. In addition, mice lacking the LPA1 receptor gene (lpa1-/- mice) lost these nerve injury-induced neuropathic pain behaviors and phenomena. However, since lpa1-/- mice did not exhibit any effects on the basal nociceptive threshold, it is possible that nerve injury-induced neuropathic pain and its machineries are initiated by LPA via defined biosynthetic pathways that involve multiple enzymes. Here, we attempted to clarify the involvement of a single synthetic enzyme of LPA known as autotaxin (ATX) in nerve injury-induced neuropathic pain. Wild-type mice with partial sciatic nerve injury showed robust mechanical allodynia starting from day 3 after the nerve injury and persisting for at least 14 days, along with thermal hyperalgesia. On the other hand, heterozygous mutant mice for the autotaxin gene (atx+/-), which have 50% ATX protein and 50% lysophospholipase D activity compared with wild-type mice, showed approximately 50% recovery of nerve injury-induced neuropathic pain. In addition, hypersensitization of myelinated AMath- or Aδ-fiber function following nerve injury was observed in electrical stimuli-induced paw withdrawal tests using a Neurometer?. The hyperalgesia was completely abolished in lpa1-/- mice, and reduced by 50% in atx+/- mice. Taken together, these findings suggest that LPA biosynthesis through ATX is the source of LPA for LPA1 receptor-mediated neuropathic pain. Therefore, targeted inhibition of ATX-mediated LPA biosynthesis as well as LPA1 receptor and its downstream pathways may represent a novel way to prevent nerve injury-induced neuropathic pain.","subitem_description_type":"Abstract"}]},"item_2_description_63":{"attribute_name":"引用","attribute_value_mlt":[{"subitem_description":"Molecular Pain, 4(6); 2008","subitem_description_type":"Other"}]},"item_2_publisher_33":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"BioMed Central"}]},"item_2_relation_11":{"attribute_name":"PubMed番号","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"18261210","subitem_relation_type_select":"PMID"}}]},"item_2_relation_12":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1186/1744-8069-4-6","subitem_relation_type_select":"DOI"}}]},"item_2_rights_13":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"c 2008 Inoue et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited."}]},"item_2_source_id_10":{"attribute_name":"書誌レコードID","attribute_value_mlt":[{"subitem_source_identifier":"AA12051230","subitem_source_identifier_type":"NCID"}]},"item_2_version_type_16":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Inoue, Makoto"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Ma, Lin"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Aoki, Junken"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Chun, Jerold"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Ueda, Hiroshi"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-12-23"}],"displaytype":"detail","filename":"MolPai4.pdf","filesize":[{"value":"403.4 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"MolPai4.pdf","url":"https://nagasaki-u.repo.nii.ac.jp/record/18202/files/MolPai4.pdf"},"version_id":"0741439e-833a-494d-afda-34ebf9714116"}]},"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":"Autotaxin, a synthetic enzyme of lysophosphatidic acid (LPA), mediates the induction of nerve-injured neuropathic pain","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Autotaxin, a synthetic enzyme of lysophosphatidic acid (LPA), mediates the induction of nerve-injured neuropathic pain"}]},"item_type_id":"2","owner":"2","path":["74"],"pubdate":{"attribute_name":"公開日","attribute_value":"2008-08-25"},"publish_date":"2008-08-25","publish_status":"0","recid":"18202","relation_version_is_last":true,"title":["Autotaxin, a synthetic enzyme of lysophosphatidic acid (LPA), mediates the induction of nerve-injured neuropathic pain"],"weko_creator_id":"2","weko_shared_id":-1},"updated":"2023-05-16T04:05:27.279987+00:00"}