rdf:type |
|
lifeskim:mentions |
umls-concept:C0014257,
umls-concept:C0038250,
umls-concept:C0332281,
umls-concept:C0535298,
umls-concept:C0600210,
umls-concept:C0600518,
umls-concept:C0871261,
umls-concept:C1100714,
umls-concept:C1439296,
umls-concept:C1527148,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2349975,
umls-concept:C2911692
|
pubmed:issue |
7
|
pubmed:dateCreated |
2011-6-16
|
pubmed:abstractText |
Deposits that accumulate beneath retinal pigment epithelium, called drusen, are early signs of age-related macular degeneration (AMD). We have shown that amyloid ? (A?) is present in drusen, and A? may be involved in AMD development. We have also shown that endothelial progenitor cells (EPCs) may contribute to the development of choroidal neovascularization (CNV). Thus, the purpose of this study was to investigate the role played by CX3CR1, a chemokine receptor, in EPC migration and CNV formation.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/CX3CL1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CX3CR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CX3CL1,
http://linkedlifedata.com/resource/pubmed/chemical/Cx3cr1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1beta,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jul
|
pubmed:issn |
1524-4636
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:volume |
31
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
e11-8
|
pubmed:meshHeading |
pubmed-meshheading:21527754-Amyloid beta-Peptides,
pubmed-meshheading:21527754-Animals,
pubmed-meshheading:21527754-Bone Marrow Transplantation,
pubmed-meshheading:21527754-Cell Movement,
pubmed-meshheading:21527754-Cell Proliferation,
pubmed-meshheading:21527754-Cells, Cultured,
pubmed-meshheading:21527754-Chemokine CX3CL1,
pubmed-meshheading:21527754-Choroidal Neovascularization,
pubmed-meshheading:21527754-Disease Models, Animal,
pubmed-meshheading:21527754-Endothelial Cells,
pubmed-meshheading:21527754-Humans,
pubmed-meshheading:21527754-Interleukin-1beta,
pubmed-meshheading:21527754-Lasers, Semiconductor,
pubmed-meshheading:21527754-Mice,
pubmed-meshheading:21527754-Mice, Inbred C57BL,
pubmed-meshheading:21527754-Mice, Knockout,
pubmed-meshheading:21527754-Receptors, Chemokine,
pubmed-meshheading:21527754-Stem Cells,
pubmed-meshheading:21527754-Tumor Necrosis Factor-alpha,
pubmed-meshheading:21527754-Up-Regulation
|
pubmed:year |
2011
|
pubmed:articleTitle |
Amyloid beta enhances migration of endothelial progenitor cells by upregulating CX3CR1 in response to fractalkine, which may be associated with development of choroidal neovascularization.
|
pubmed:affiliation |
Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|