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TLR2-induced astrocyte MMP9 activation compromises the blood brain barrier and exacerbates intracerebral hemorrhage in animal models

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dc.contributor.authorMin, Hyunjung-
dc.contributor.authorHong, Jinpyo-
dc.contributor.authorCho, Ik-Hyun-
dc.contributor.authorJang, Yong Ho-
dc.contributor.authorLee, Hyunkyoung-
dc.contributor.authorKim, Dongwoon-
dc.contributor.authorYu, Seong-Woon-
dc.contributor.authorLee, Soojin-
dc.contributor.authorLee, Sung Joong-
dc.date.accessioned2017-03-17T07:51:46Z-
dc.date.available2017-03-17T17:18:20Z-
dc.date.issued2015-04-10-
dc.identifier.citationMolecular Brain. 2015 Apr 10;8(1):23ko_KR
dc.identifier.urihttps://hdl.handle.net/10371/109819-
dc.description.abstractBackground
The innate immune response plays an important role in the pathogenesis of intracerebral hemorrhage (ICH). Recent studies have shown that Toll-like receptor 2 (TLR2) is involved in the innate immune response in various neurological diseases, yet neither its role in ICH nor the mechanisms by which it functions have yet been elucidated. We examined these in this study using a collagenase-induced mouse ICH model with TLR2 knock-out (KO) mice.

Results
TLR2 expression was upregulated in the ipsilateral hemorrhagic tissues of the collagenase-injected mice. Brain injury volume and neurological deficits following ICH were reduced in TLR2 KO mice compared to wild-type (WT) control mice. Heterologous blood-transfer experiments show that TLR2 signaling in brain-resident cells, but not leukocytes, contributes to the injury. In our study to elucidate underlying mechanisms, we found that damage to blood–brain barrier (BBB) integrity following ICH was attenuated in TLR2 KO mice compared to WT mice, which may be due to reduced matrix metalloproteinase-9 (MMP9) activation in astrocytes. The reduced BBB damage accompanies decreased neutrophil infiltration and proinflammatory gene expression in the injured brain parenchyma, which may account for the attenuated brain damage in TLR2 KO mice after ICH.

Conclusions
TLR2 plays a detrimental role in ICH-induced brain damage by activating MMP9 in astrocytes, compromising BBB, and enhancing neutrophils infiltration and proinflammatory gene expression.
ko_KR
dc.language.isoenko_KR
dc.publisherBioMed Centralko_KR
dc.subjectToll-like receptorko_KR
dc.subjectStrokeko_KR
dc.subjectNeuroinflammationko_KR
dc.subjectNeutrophilko_KR
dc.subjectMatrix metalloproteinase-9ko_KR
dc.titleTLR2-induced astrocyte MMP9 activation compromises the blood brain barrier and exacerbates intracerebral hemorrhage in animal modelsko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor민현정-
dc.contributor.AlternativeAuthor홍진표-
dc.contributor.AlternativeAuthor조익현-
dc.contributor.AlternativeAuthor장용호-
dc.contributor.AlternativeAuthor이현경-
dc.contributor.AlternativeAuthor김동운-
dc.contributor.AlternativeAuthor유성운-
dc.contributor.AlternativeAuthor이수진-
dc.contributor.AlternativeAuthor이성중-
dc.identifier.doi10.1186/s13041-015-0116-z-
dc.language.rfc3066en-
dc.rights.holderMin et al.; licensee BioMed Central.-
dc.date.updated2017-01-06T10:35:11Z-
Appears in Collections:
College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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