BMS-986020, a Specific LPA(1) Antagonist, Provides Neuroprotection against Ischemic Stroke in Mice
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Gaire, B.P. | - |
dc.contributor.author | Sapkota, A. | - |
dc.contributor.author | Choi, J.W. | - |
dc.date.available | 2020-11-30T05:40:20Z | - |
dc.date.created | 2020-11-16 | - |
dc.date.issued | 2020-11 | - |
dc.identifier.issn | 2076-3921 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/79120 | - |
dc.description.abstract | Stroke is a leading cause of death. Stroke survivors often suffer from long-term functional disability. This study demonstrated neuroprotective effects of BMS-986020 (BMS), a selective lysophosphatidic acid receptor 1 (LPA1) antagonist under clinical trials for lung fibrosis and psoriasis, against both acute and sub-acute injuries after ischemic stroke by employing a mouse model with transient middle cerebral artery occlusion (tMCAO). BMS administration immediately after reperfusion significantly attenuated acute brain injuries including brain infarction, neurological deficits, and cell apoptosis at day 1 after tMCAO. Neuroprotective effects of BMS were preserved even when administered at 3 h after reperfusion. Neuroprotection by BMS against acute injuries was associated with attenuation of microglial activation and lipid peroxidation in post-ischemic brains. Notably, repeated BMS administration daily for 14 days after tMCAO exerted long-term neuroprotection in tMCAO-challenged mice, as evidenced by significantly attenuated neurological deficits and improved survival rate. It also attenuated brain tissue loss and cell apoptosis in post-ischemic brains. Mechanistically, it significantly enhanced neurogenesis and angiogenesis in injured brains. A single administration of BMS provided similar long-term neuroprotection except survival rate. Collectively, BMS provided neuroprotection against both acute and sub-acute injuries of ischemic stroke, indicating that BMS might be an appealing therapeutic agent to treat ischemic stroke. © 2020 by the authors. Licensee MDPI, Basel, Switzerland. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI AG | - |
dc.relation.isPartOf | Antioxidants | - |
dc.title | BMS-986020, a Specific LPA(1) Antagonist, Provides Neuroprotection against Ischemic Stroke in Mice | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000592958300001 | - |
dc.identifier.doi | 10.3390/antiox9111097 | - |
dc.identifier.bibliographicCitation | Antioxidants, v.9, no.11, pp.1 - 14 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85095860870 | - |
dc.citation.endPage | 14 | - |
dc.citation.startPage | 1 | - |
dc.citation.title | Antioxidants | - |
dc.citation.volume | 9 | - |
dc.citation.number | 11 | - |
dc.contributor.affiliatedAuthor | Gaire, B.P. | - |
dc.contributor.affiliatedAuthor | Sapkota, A. | - |
dc.contributor.affiliatedAuthor | Choi, J.W. | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Angiogenesis | - |
dc.subject.keywordAuthor | BMS-986020 | - |
dc.subject.keywordAuthor | Long-term neuroprotection | - |
dc.subject.keywordAuthor | Neurogenesis | - |
dc.subject.keywordAuthor | Neuroprotective effects | - |
dc.subject.keywordAuthor | Transient middle cerebral artery occlusion (tMCAO) | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
1342, Seongnam-daero, Sujeong-gu, Seongnam-si, Gyeonggi-do, Republic of Korea(13120)031-750-5114
COPYRIGHT 2020 Gachon University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.