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Repair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes.

DC Field Value Language
dc.contributor.authorJeong, HK-
dc.contributor.authorJi, KM-
dc.contributor.authorKim, J-
dc.contributor.authorJou, I-
dc.contributor.authorJoe, EH-
dc.date.accessioned2014-04-30T04:45:07Z-
dc.date.available2014-04-30T04:45:07Z-
dc.date.issued2013-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/9874-
dc.description.abstractInflammation in injured tissue has both repair functions and cytotoxic consequences. However, the issue of whether brain inflammation has a repair function has received little attention. Previously, we demonstrated monocyte infiltration and death of neurons and resident microglia in LPS-injected brains (Glia. 2007. 55:1577; Glia. 2008. 56:1039). Here, we found that astrocytes, oligodendrocytes, myelin, and endothelial cells disappeared in the damage core within 1-3 d and then re-appeared at 7-14 d, providing evidence of repair of the brain microenvironment. Since round Iba-1+/CD45+ monocytes infiltrated before the repair, we examined whether these cells were involved in the repair process. Analysis of mRNA expression profiles showed significant upregulation of repair/resolution-related genes, whereas proinflammatory-related genes were barely detectable at 3 d, a time when monocytes filled injury sites. Moreover, Iba-1+/CD45+ cells highly expressed phagocytic activity markers (e.g., the mannose receptors, CD68 and LAMP2), but not proinflammatory mediators (e.g., iNOS and IL1β). In addition, the distribution of round Iba-1+/CD45+ cells was spatially and temporally correlated with astrocyte recovery. We further found that monocytes in culture attracted astrocytes by releasing soluble factor(s). Together, these results suggest that brain inflammation mediated by monocytes functions to repair the microenvironment of the injured brain.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHAstrocytes/drug effects/*pathology-
dc.subject.MESHBlood Vessels/drug effects/*pathology-
dc.subject.MESHBrain Injuries/*blood/*pathology/physiopathology-
dc.subject.MESHCell Movement/drug effects-
dc.subject.MESHCell Proliferation/drug effects-
dc.subject.MESHEndothelial Cells/drug effects/pathology-
dc.subject.MESHInflammation/pathology-
dc.subject.MESHKi-67 Antigen/metabolism-
dc.subject.MESHLipopolysaccharides/pharmacology-
dc.subject.MESHMale-
dc.subject.MESHMonocytes/drug effects/*metabolism-
dc.subject.MESHMyelin Sheath/*metabolism-
dc.subject.MESHNeurites/drug effects/pathology-
dc.subject.MESHOligonucleotide Array Sequence Analysis-
dc.subject.MESHRNA, Messenger/genetics/metabolism-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHRecovery of Function/drug effects-
dc.subject.MESHSubstantia Nigra/drug effects/pathology/physiopathology-
dc.subject.MESH*Wound Healing/drug effects-
dc.titleRepair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes.-
dc.typeArticle-
dc.identifier.pmid23758980-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684510/-
dc.contributor.affiliatedAuthor주, 일로-
dc.contributor.affiliatedAuthor조, 은혜-
dc.type.localJournal Papers-
dc.identifier.doi10.1186/1756-6606-6-28-
dc.citation.titleMolecular brain-
dc.citation.volume6-
dc.citation.date2013-
dc.citation.startPage28-
dc.citation.endPage28-
dc.identifier.bibliographicCitationMolecular brain, 6:28-28, 2013-
dc.identifier.eissn1756-6606-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
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