Chronic Cerebral Hypoperfusion Induces Alterations of Matrix Metalloproteinase-9 and Angiopoietin-2 Levels in the Rat Hippocampus

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dc.contributor.authorKim, Min-Sooen
dc.contributor.authorChoi, Bo-Ryoungen
dc.contributor.authorLee, Yong Wooen
dc.contributor.authorKim, Dong-Heeen
dc.contributor.authorHan, Ye Sunen
dc.contributor.authorJeon, Won Kyungen
dc.contributor.authorHan, Jung-Sooen
dc.date.accessioned2019-09-05T17:12:00Zen
dc.date.available2019-09-05T17:12:00Zen
dc.date.issued2018-08en
dc.description.abstractAngiogenic factors contribute to cerebral angiogenesis following cerebral hypoperfusion, and understanding these temporal changes is essential to developing effective treatments. The present study examined temporal alterations in angiogenesis-related matrix metalloproteinase-9 (MMP-9) and angiopoietin-2 (ANG-2) expression in the hippocampus following bilateral common carotid artery occlusion (BCCAo). Male Wistar rats (12 weeks of age) were randomly assigned to sham-operated control or experimental groups, and expression levels of MMP-9 and ANG-2 were assessed after BCCAo (1 week, 4 weeks, and 8 weeks), using western blotting. Protein expression increased 1 week after BCCAo and returned to control levels at 4 and 8 weeks. In addition, immunofluorescence staining demonstrated that the MMP-9- and ANG-2-positive signals were primarily observed in the NeuN-positive neurons with very little labeling in non-neuronal cells and no labeling in endothelial cells. In addition, these cellular locations of MMP-9-and ANG-2-positive signals were not altered over time following BCCAo. Other angiogenic factors such as vascular endothelial growth factor and hypoxia-inducible factor did not differ from controls at 1 week; however, expression of both factors increased at 4 and 8 weeks in the BCCAo group compared to the control group. Our findings increase understanding of alterations in angiogenic factors during the progression of cerebral angiogenesis and are relevant to developing effective temporally based therapeutic strategies for chronic cerebral hypoperfusion-associated neurological disorders such as vascular dementia.en
dc.description.notesThis work was funded by the R & D Convergence Program of the Republic of Korea National Research Council of Science & Technology (grant numbers CRC-15-04-KIST, G15120, G16230, K16850 and K17850) and the Korea Health Technology R & D Project, through the Korea Health Industry Development Institute (KHIDI), which is funded by the Ministry of Health & Welfare, Republic of Korea (grant number HI15C1540).en
dc.description.sponsorshipR & D Convergence Program of the Republic of Korea National Research Council of Science Technology [CRC-15-04-KIST, G15120, G16230, K16850, K17850]; Korea Health Technology R & D Project, through the Korea Health Industry Development Institute (KHIDI); Ministry of Health & Welfare, Republic of Korea [HI15C1540]en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.5607/en.2018.27.4.299en
dc.identifier.eissn2093-8144en
dc.identifier.issn1226-2560en
dc.identifier.issue4en
dc.identifier.pmid30181692en
dc.identifier.urihttp://hdl.handle.net/10919/93398en
dc.identifier.volume27en
dc.language.isoenen
dc.rightsCreative Commons Attribution-NonCommercial 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/en
dc.subjectBCCAoen
dc.subjectAngiogenesisen
dc.subjectAngiopoietin-2en
dc.subjectMatrix metalloproteinase-9en
dc.subjectVascular dementiaen
dc.titleChronic Cerebral Hypoperfusion Induces Alterations of Matrix Metalloproteinase-9 and Angiopoietin-2 Levels in the Rat Hippocampusen
dc.title.serialExperimental Neurobiologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.dcmitypeStillImageen

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