| pubmed-article:7635947 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7635947 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:7635947 | lifeskim:mentions | umls-concept:C0005961 | lld:lifeskim |
| pubmed-article:7635947 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:7635947 | lifeskim:mentions | umls-concept:C0020443 | lld:lifeskim |
| pubmed-article:7635947 | lifeskim:mentions | umls-concept:C0003591 | lld:lifeskim |
| pubmed-article:7635947 | lifeskim:mentions | umls-concept:C0205082 | lld:lifeskim |
| pubmed-article:7635947 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:7635947 | pubmed:dateCreated | 1995-9-11 | lld:pubmed |
| pubmed-article:7635947 | pubmed:abstractText | Apo E, a key regulator of cholesterol-rich lipoprotein metabolism, is synthesized by numerous extrahepatic tissues. Although its synthesis in macrophages is documented, the contribution of macrophage-derived apo E to hepatic clearance of serum cholesterol is unknown. To address this issue bone marrow transplantation was performed on hypercholesterolemic apo E-deficient mice with either syngeneic apo E-deficient mouse bone marrow cells (E0-control) or wild-type mouse bone marrow cells expressing apo E (E0-treated). E0-control and E0-treated mice were fed either a regular chow diet or an atherogenic diet (designated E0-control-HF and E0-treated-HF). Serum cholesterol levels dropped dramatically in the E0-treated mice largely due to a reduction in their VLDL cholesterol. No changes were seen in the E0-control mice. After 4 wk serum cholesterol in E0-treated-HF mice was about four-fold lower compared to E0-control-HF animals. Moreover, the extent of atherosclerosis in the E0-treated-HF mice after 14-16 wk was greatly reduced. Wild-type apo E mRNA was detected in the liver, spleen, and brain of the E0-treated mice indicating that apo E gene transfer was successfully achieved through bone marrow transplantation. More importantly, the level of apo E expression was sufficient to reduce the severe hypercholesterolemia of the apo E-deficient mice fed either chow or atherogenic diets. | lld:pubmed |
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| pubmed-article:7635947 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7635947 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7635947 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:7635947 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7635947 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:7635947 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:7635947 | pubmed:author | pubmed-author:CurtissL KLK | lld:pubmed |
| pubmed-article:7635947 | pubmed:author | pubmed-author:SpangenbergJJ | lld:pubmed |
| pubmed-article:7635947 | pubmed:author | pubmed-author:BoisvertW AWA | lld:pubmed |
| pubmed-article:7635947 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7635947 | pubmed:volume | 96 | lld:pubmed |
| pubmed-article:7635947 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7635947 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7635947 | pubmed:pagination | 1118-24 | lld:pubmed |
| pubmed-article:7635947 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7635947 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7635947 | pubmed:articleTitle | Treatment of severe hypercholesterolemia in apolipoprotein E-deficient mice by bone marrow transplantation. | lld:pubmed |
| pubmed-article:7635947 | pubmed:affiliation | Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA. | lld:pubmed |
| pubmed-article:7635947 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7635947 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7635947 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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