| pubmed-article:7911126 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0072108 | lld:lifeskim |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0160680 | lld:lifeskim |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0020507 | lld:lifeskim |
| pubmed-article:7911126 | lifeskim:mentions | umls-concept:C0028953 | lld:lifeskim |
| pubmed-article:7911126 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:7911126 | pubmed:dateCreated | 1994-7-7 | lld:pubmed |
| pubmed-article:7911126 | pubmed:abstractText | We have used antisense phosphorothioate oligonucleotides to define the role played by proliferating cell nuclear antigen (PCNA) in neointimal accumulation of smooth muscle cells in a rat carotid artery injury model. The short-term extraluminal delivery of 250 nmol of antisense oligonucleotides, but not control oligonucleotides, immediately after arterial injury produces a 77% suppression of PCNA mRNA after 24 h and a 52% decrease in the frequency of medial smooth muscle cells expressing PCNA after 72 h. This reduction in PCNA expression is accompanied by a 59% decrease in the frequency of proliferating medial smooth muscle cells at 3 d as measured by BudR staining and an 80% decrease in neointimal accumulation assessed morphometrically at 2 wk. Thus, the expression of PCNA is required for medial smooth muscle cell growth in vivo and for neointimal formation after arterial injury. | lld:pubmed |
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| pubmed-article:7911126 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7911126 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:7911126 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7911126 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:7911126 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:7911126 | pubmed:author | pubmed-author:RosenbergR... | lld:pubmed |
| pubmed-article:7911126 | pubmed:author | pubmed-author:SimonsMM | lld:pubmed |
| pubmed-article:7911126 | pubmed:author | pubmed-author:EdelmanE RER | lld:pubmed |
| pubmed-article:7911126 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7911126 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:7911126 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7911126 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7911126 | pubmed:pagination | 2351-6 | lld:pubmed |
| pubmed-article:7911126 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7911126 | pubmed:meshHeading | pubmed-meshheading:7911126-... | lld:pubmed |
| pubmed-article:7911126 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7911126 | pubmed:articleTitle | Antisense proliferating cell nuclear antigen oligonucleotides inhibit intimal hyperplasia in a rat carotid artery injury model. | lld:pubmed |
| pubmed-article:7911126 | pubmed:affiliation | Department of Biology, Massachusetts Institute of Technology, Cambridge 02139. | lld:pubmed |
| pubmed-article:7911126 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7911126 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7911126 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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