Linked Life Data

21042291

Source:http://linkedlifedata.com/resource/pubmed/id/21042291

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-3-30
pubmed:abstractText
Tissue factor (TF) is the primary initiator of blood coagulation. In addition to hemostasis, TF can initiate intracellular signaling and promote inflammation and angiogenesis, the key processes underlying the pathogenesis of age-related macular degeneration (AMD). AMD, the leading cause of irreversible blindness among the elderly, involves many genetic and environmental risk factors, including oxidative stress and inflammation. In this study, TF expression was examined in human AMD tissue and in the eyes of a model of AMD, the Ccl2(-/-)/Cx3cr1(-/-) (DKO) mouse, as well as in the ARPE-19 cell line after lipopolysaccharide (LPS) and H(2)O(2) stimulation. Total RNA was extracted from tissue samples and further analyzed by real-time RT-PCR. Immunohistochemistry was performed to evaluate TF protein expression. In the human retina, a 32-fold increase of TF mRNA expression was detected in AMD macular lesions compared with normal maculae. TF protein expression was also enhanced in human AMD maculae. Similarly, TF transcript and protein expression were moderately increased in retinal lesions, neuroretinal tissue, and cultured RPE cells of DKO mice compared with age-matched wild-type mice. TF expression level correlated with age in both wild-type and DKO mice. In order to better understand how AMD might lead to enhanced TF expression, 1, 5, and 10 ?g/ml LPS as well as 100 and 200 ?M H(2)O(2) were used to stimulate ARPE-19 cells for 24 and 2 h, respectively. LPS treatment consistently increased TF transcript and protein expression. H(2)O(2) alone or in combination with LPS also moderately enhanced TF expression. These results indicate that upregulated TF expression may be associated with AMD, and inflammatory and oxidative stress may contribute to TF expression in AMD eyes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1530-0307
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
519-26
pubmed:dateRevised
2011-10-3
pubmed:meshHeading
pubmed-meshheading:21042291-Aging, pubmed-meshheading:21042291-Animals, pubmed-meshheading:21042291-Cells, Cultured, pubmed-meshheading:21042291-Chemokine CCL2, pubmed-meshheading:21042291-Drug Combinations, pubmed-meshheading:21042291-Humans, pubmed-meshheading:21042291-Hydrogen Peroxide, pubmed-meshheading:21042291-Lipopolysaccharides, pubmed-meshheading:21042291-Macula Lutea, pubmed-meshheading:21042291-Macular Degeneration, pubmed-meshheading:21042291-Mice, pubmed-meshheading:21042291-Mice, Inbred C57BL, pubmed-meshheading:21042291-Mice, Knockout, pubmed-meshheading:21042291-Oxidative Stress, pubmed-meshheading:21042291-RNA, Messenger, pubmed-meshheading:21042291-Receptors, Chemokine, pubmed-meshheading:21042291-Retina, pubmed-meshheading:21042291-Retinal Pigment Epithelium, pubmed-meshheading:21042291-Thromboplastin, pubmed-meshheading:21042291-Up-Regulation
pubmed:year
2011
pubmed:articleTitle
Evidence for enhanced tissue factor expression in age-related macular degeneration.
pubmed:affiliation
Immunopathology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-1857, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, N.I.H., Intramural