Overexpression of Human S100B Exacerbates Brain Damage and Periinfarct Gliosis After Permanent Focal Ischemia

We have previously demonstrated that augmented and prolonged activation of astrocytes detrimentally influences both the subacute and chronic phases of cerebral ischemia. Furthermore, we have suggested that the astrocyte-derived protein S100B may be important in these pathogenic events. However, the...

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Veröffentlicht in:Stroke (1970) 2008-07, Vol.39 (7), p.2114-2121
Hauptverfasser: MORI, Takashi, JUN TAN, ARENDASH, Gary W, KOYAMA, Naoki, NOJIMA, Yoshiko, TOWN, Terrence
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container_end_page 2121
container_issue 7
container_start_page 2114
container_title Stroke (1970)
container_volume 39
creator MORI, Takashi
JUN TAN
ARENDASH, Gary W
KOYAMA, Naoki
NOJIMA, Yoshiko
TOWN, Terrence
description We have previously demonstrated that augmented and prolonged activation of astrocytes detrimentally influences both the subacute and chronic phases of cerebral ischemia. Furthermore, we have suggested that the astrocyte-derived protein S100B may be important in these pathogenic events. However, the causal relationship between S100B and exacerbation of brain damage in vivo remains to be elucidated. Using transgenic mice overexpressing human S100B (Tg huS100B mice), we examined whether S100B plays a cardinal role in aggravation of brain damage after permanent middle cerebral artery occlusion (pMCAO). Tg huS100B mice had significantly larger infarct volumes and worse neurological deficits at any time point examined after pMCAO as compared with CD-1 background strain-matched control mice. Infarct volumes in Tg huS100B mice were significantly increased from 1 to 3 and 5 days after pMCAO (delayed infarct expansion), whereas those in control mice were not significantly altered. S100, glial fibrillary acidic protein, and Iba1 burdens in the periinfarct area were significantly increased through to 7 days after pMCAO in Tg huS100B mice, whereas those in control mice reached a plateau at 3 days after pMCAO. These results provide genetic evidence that overexpression of human S100B acts to exacerbate brain damage and periinfarct reactive gliosis (astrocytosis and microgliosis) during the subacute phase of pMCAO.
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Furthermore, we have suggested that the astrocyte-derived protein S100B may be important in these pathogenic events. However, the causal relationship between S100B and exacerbation of brain damage in vivo remains to be elucidated. Using transgenic mice overexpressing human S100B (Tg huS100B mice), we examined whether S100B plays a cardinal role in aggravation of brain damage after permanent middle cerebral artery occlusion (pMCAO). Tg huS100B mice had significantly larger infarct volumes and worse neurological deficits at any time point examined after pMCAO as compared with CD-1 background strain-matched control mice. Infarct volumes in Tg huS100B mice were significantly increased from 1 to 3 and 5 days after pMCAO (delayed infarct expansion), whereas those in control mice were not significantly altered. S100, glial fibrillary acidic protein, and Iba1 burdens in the periinfarct area were significantly increased through to 7 days after pMCAO in Tg huS100B mice, whereas those in control mice reached a plateau at 3 days after pMCAO. 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S100, glial fibrillary acidic protein, and Iba1 burdens in the periinfarct area were significantly increased through to 7 days after pMCAO in Tg huS100B mice, whereas those in control mice reached a plateau at 3 days after pMCAO. These results provide genetic evidence that overexpression of human S100B acts to exacerbate brain damage and periinfarct reactive gliosis (astrocytosis and microgliosis) during the subacute phase of pMCAO.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Injuries - diagnosis</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Ischemia - diagnosis</subject><subject>Brain Ischemia - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Gliosis - pathology</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Infarction, Middle Cerebral Artery - genetics</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Nerve Growth Factors - biosynthesis</subject><subject>Neurology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Pharmacology. 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Drug treatments</topic><topic>S100 Calcium Binding Protein beta Subunit</topic><topic>S100 Proteins - biosynthesis</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MORI, Takashi</creatorcontrib><creatorcontrib>JUN TAN</creatorcontrib><creatorcontrib>ARENDASH, Gary W</creatorcontrib><creatorcontrib>KOYAMA, Naoki</creatorcontrib><creatorcontrib>NOJIMA, Yoshiko</creatorcontrib><creatorcontrib>TOWN, Terrence</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MORI, Takashi</au><au>JUN TAN</au><au>ARENDASH, Gary W</au><au>KOYAMA, Naoki</au><au>NOJIMA, Yoshiko</au><au>TOWN, Terrence</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of Human S100B Exacerbates Brain Damage and Periinfarct Gliosis After Permanent Focal Ischemia</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2008-07-01</date><risdate>2008</risdate><volume>39</volume><issue>7</issue><spage>2114</spage><epage>2121</epage><pages>2114-2121</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>We have previously demonstrated that augmented and prolonged activation of astrocytes detrimentally influences both the subacute and chronic phases of cerebral ischemia. 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source MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Alma/SFX Local Collection
subjects Animals
Biological and medical sciences
Brain - metabolism
Brain - pathology
Brain Injuries - diagnosis
Brain Injuries - metabolism
Brain Ischemia - diagnosis
Brain Ischemia - metabolism
Gene Expression Regulation
Gliosis - pathology
Homozygote
Humans
Infarction, Middle Cerebral Artery - genetics
Infarction, Middle Cerebral Artery - metabolism
Male
Medical sciences
Mice
Mice, Transgenic
Nerve Growth Factors - biosynthesis
Neurology
Neuropharmacology
Neuroprotective agent
Pharmacology. Drug treatments
S100 Calcium Binding Protein beta Subunit
S100 Proteins - biosynthesis
Vascular diseases and vascular malformations of the nervous system
title Overexpression of Human S100B Exacerbates Brain Damage and Periinfarct Gliosis After Permanent Focal Ischemia
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