rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
2
|
pubmed:dateCreated |
1992-3-18
|
pubmed:abstractText |
Apo E plays an important role in plasma lipoprotein metabolism through its high affinity binding to cell surface LDL receptor. In the present study, we studied the effects of apo E on the atherogenic process in Watanabe heritable hyperlipidemic rabbits which are deficient in LDL receptor and an animal model for familial hypercholesterolemia. We isolated apo E from plasma of 1% cholesterol-fed rabbits and administered 10 mg of purified apo E intravenously into five Watanabe heritable hyperlipidemic rabbits three times a week from their age of 2.5 months to 11 months for 8.5 months. After sustained administration to apo E, we found a significant reduction in the accumulation of cholesterol ester in aortae (1.55 +/- 0.07 mg/g tissue) as compared to control rabbits (4.32 +/- 0.61 mg/g tissue). Supporting this, the percentage of the surface area of the aorta with macroscopic plaque was remarkably decreased in apo E-treated animals (18.8 +/- 5.1% vs. 38.8 +/- 8.0% in control). Thus, apo E definitely prevented the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbits.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-1698775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-1849015,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-1993681,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-2303437,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-2384229,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-2594771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-2723074,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-2911597,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3198768,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3266596,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3283935,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3290249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3458191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3475709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3478721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3576212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3593072,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3611356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3625036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3778306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-3918303,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-4703655,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-4818200,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-6282937,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-6343371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-6823554,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-6950395,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-6960858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-7406953,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1737858-7440569
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
0021-9738
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
89
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
N
|
pubmed:pagination |
706-11
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
|
pubmed:year |
1992
|
pubmed:articleTitle |
Apolipoprotein E prevents the progression of atherosclerosis in Watanabe heritable hyperlipidemic rabbits.
|
pubmed:affiliation |
3rd Department of Internal Medicine, University of Tokyo, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|