rdf:type |
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0023821,
umls-concept:C0024432,
umls-concept:C0026473,
umls-concept:C0032105,
umls-concept:C0185117,
umls-concept:C0441889,
umls-concept:C0547040,
umls-concept:C1412058,
umls-concept:C1880177,
umls-concept:C2911684
|
pubmed:issue |
9
|
pubmed:dateCreated |
2001-11-6
|
pubmed:abstractText |
Excess accumulation of cholesterol in macrophages results in foam cell production and lesion development. Recent studies have demonstrated that ATP-binding cassette protein A1 (ABCA1) is highly regulated in macrophages and mediates the efflux of cholesterol and phospholipids to apolipoproteins, a process necessary for HDL formation. The goal of this study was to determine the contribution of monocyte/macrophage ABCA1 to HDL formation in vivo. We generated mice expressing ABCA1 in macrophages and mice with selected inactivation of ABCA1 in macrophages by bone marrow transplantation in ABCA1-deficient (ABC1(-/-)) and wild-type (WT) mice. At all times, the level of HDL in ABC1(-/-) recipient mice remained low relative to WT recipient mice irrespective of the genotype of the donor macrophage ABCA1 or high-fat feeding. Expression of WT macrophage ABCA1 in ABC1(-/-) mice resulted in a small but significant increase in apoA-I levels starting 2 weeks after transplantation. No further increase in apoAI was observed up to 14 weeks after transplantation. The increase in apoAI was accompanied by a small but significant increase in HDL cholesterol 6 weeks after transplantation. The HDL formed as a consequence of the expression of WT macrophage ABCA1 migrated to the alpha position in a two-dimensional gel electrophoresis. These results demonstrate that monocyte/macrophage ABCA1 contributes to HDL formation; however, the contribution to the overall plasma HDL levels is minimal.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10079112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10092505,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10224147,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10364084,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10431236,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10431237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10431238,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10525055,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10760292,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-10893411,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-11696569,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-182724,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-6796585,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-7635947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-7751809,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-8449981,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-8479518,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-8808761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-9114045,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-9144096,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-9188474,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-9242527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-9261096,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11696576-9799800
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
0021-9738
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
108
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1315-20
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:11696576-ATP-Binding Cassette Transporters,
pubmed-meshheading:11696576-Animals,
pubmed-meshheading:11696576-Bone Marrow Transplantation,
pubmed-meshheading:11696576-Crosses, Genetic,
pubmed-meshheading:11696576-Electrophoresis, Gel, Two-Dimensional,
pubmed-meshheading:11696576-Humans,
pubmed-meshheading:11696576-Lipoproteins, HDL,
pubmed-meshheading:11696576-Macrophages,
pubmed-meshheading:11696576-Macrophages, Peritoneal,
pubmed-meshheading:11696576-Mice,
pubmed-meshheading:11696576-Monocytes,
pubmed-meshheading:11696576-Protein Binding,
pubmed-meshheading:11696576-Tangier Disease,
pubmed-meshheading:11696576-Time Factors
|
pubmed:year |
2001
|
pubmed:articleTitle |
Monocyte/macrophage expression of ABCA1 has minimal contribution to plasma HDL levels.
|
pubmed:affiliation |
Pfizer Global Research and Development, Groton, Connecticut 06340, USA.
|
pubmed:publicationType |
Journal Article
|