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Elucidation of Relevant Neuroinflammation Mechanisms Using Gene Expression Profiling in Patients with Amyotrophic Lateral Sclerosis

DC Field Value Language
dc.contributor.author강성웅-
dc.contributor.author김도영-
dc.contributor.author김형범-
dc.contributor.author조성래-
dc.contributor.author최영철-
dc.contributor.author하윤-
dc.date.accessioned2017-10-26T07:52:57Z-
dc.date.available2017-10-26T07:52:57Z-
dc.date.issued2016-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/152638-
dc.description.abstractAmyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by damage of motor neurons. Recent reports indicate that inflammatory responses occurring within the central nervous system contribute to the pathogenesis of ALS. We aimed to investigate disease-specific gene expression associated with neuroinflammation by conducting transcriptome analysis on fibroblasts from three patients with sporadic ALS and three normal controls. Several pathways were found to be upregulated in patients with ALS, among which the toll-like receptor (TLR) and NOD-like receptor (NLR) signaling pathways are related to the immune response. Genes-toll-interacting protein (TOLLIP), mitogen-activated protein kinase 9 (MAPK9), interleukin-1β (IL-1β), interleukin-8 (IL-8), and chemokine (C-X-C motif) ligand 1 (CXCL1)-related to these two pathways were validated using western blotting. This study validated the genes that are associated with TLR and NLR signaling pathways from different types of patient-derived cells. Not only fibroblasts but also induced pluripotent stem cells (iPSCs) and neural rosettes from the same origins showed similar expression patterns. Furthermore, expression of TOLLIP, a regulator of TLR signaling pathway, decreased with cellular aging as judged by changes in its expression through multiple passages. TOLLIP expression was downregulated in ALS cells under conditions of inflammation induced by lipopolysaccharide. Our data suggest that the TLR and NLR signaling pathways are involved in pathological innate immunity and neuroinflammation associated with ALS and that TOLLIP, MAPK9, IL-1β, IL-8, and CXCL1 play a role in ALS-specific immune responses. Moreover, changes of TOLLIP expression might be associated with progression of ALS.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherPublic Library of Science-
dc.relation.isPartOfPLOS ONE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleElucidation of Relevant Neuroinflammation Mechanisms Using Gene Expression Profiling in Patients with Amyotrophic Lateral Sclerosis-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Rehabilitation Medicine-
dc.contributor.googleauthorYu Hui Won-
dc.contributor.googleauthorMin-Young Lee-
dc.contributor.googleauthorYoung-Chul Choi-
dc.contributor.googleauthorYoon Ha-
dc.contributor.googleauthorHyongbum Kim-
dc.contributor.googleauthorDo-Young Kim-
dc.contributor.googleauthorMyung-Sun Kim-
dc.contributor.googleauthorJi Hea Yu-
dc.contributor.googleauthorJung Hwa Seo-
dc.contributor.googleauthorMinGi Kim-
dc.contributor.googleauthorSung-Rae Cho-
dc.contributor.googleauthorSeong-Woong Kang-
dc.identifier.doi10.1371/journal.pone.0165290-
dc.contributor.localIdA00385-
dc.contributor.localIdA01148-
dc.contributor.localIdA03831-
dc.contributor.localIdA04116-
dc.contributor.localIdA04255-
dc.contributor.localIdA00041-
dc.relation.journalcodeJ02540-
dc.identifier.eissn1932-6203-
dc.identifier.pmid27812125-
dc.contributor.alternativeNameKang, Seong Woong-
dc.contributor.alternativeNameKim, Do Young-
dc.contributor.alternativeNameKim, Hyongbum-
dc.contributor.alternativeNameCho, Sung Rae-
dc.contributor.alternativeNameChoi, Young Chul-
dc.contributor.alternativeNameHa, Yoon-
dc.contributor.affiliatedAuthorKim, Do Young-
dc.contributor.affiliatedAuthorKim, Hyongbum-
dc.contributor.affiliatedAuthorCho, Sung Rae-
dc.contributor.affiliatedAuthorChoi, Young Chul-
dc.contributor.affiliatedAuthorHa, Yoon-
dc.contributor.affiliatedAuthorKang, Seong Woong-
dc.citation.volume11-
dc.citation.number11-
dc.citation.startPagee0165290-
dc.identifier.bibliographicCitationPLOS ONE, Vol.11(11) : e0165290, 2016-
dc.date.modified2017-10-24-
dc.identifier.rimsid39647-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurosurgery (신경외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Rehabilitation Medicine (재활의학교실) > 1. Journal Papers

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