Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-5-19
pubmed:abstractText
The ability of microglial cells (MG) and macrophages (MAC) to release cytokines, induce apoptosis, as well as perform phagocytic functions suggests a possible role in wound healing following oxygen-induced injury. This study was performed to determine the temporal and spatial expression of F4/80 (F4/80+) positive microglia/macrophages (MG/MAC) in areas of retinal damage in the mouse model of oxygen-induced retinopathy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1090-0535
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
467-77
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16710171-Animals, pubmed-meshheading:16710171-Animals, Newborn, pubmed-meshheading:16710171-Antigens, Differentiation, pubmed-meshheading:16710171-Cell Proliferation, pubmed-meshheading:16710171-Chemokine CCL2, pubmed-meshheading:16710171-Ischemia, pubmed-meshheading:16710171-Macrophages, pubmed-meshheading:16710171-Mice, pubmed-meshheading:16710171-Mice, Inbred C57BL, pubmed-meshheading:16710171-Microglia, pubmed-meshheading:16710171-Neovascularization, Physiologic, pubmed-meshheading:16710171-Oxygen, pubmed-meshheading:16710171-RNA, Messenger, pubmed-meshheading:16710171-Retina, pubmed-meshheading:16710171-Retinal Diseases, pubmed-meshheading:16710171-Retinal Vessels, pubmed-meshheading:16710171-Time Factors, pubmed-meshheading:16710171-Tissue Distribution, pubmed-meshheading:16710171-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Microglia and macrophages are increased in response to ischemia-induced retinopathy in the mouse retina.
pubmed:affiliation
Department of Pediatrics, Casey Eye Institute, Oregon Health and Science University, Portland, OR 97239, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural