| pubmed-article:9409314 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0023825 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0030190 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0065058 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C1158770 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:9409314 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:9409314 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:9409314 | pubmed:dateCreated | 1998-1-22 | lld:pubmed |
| pubmed-article:9409314 | pubmed:abstractText | The hypothesized relationships between plasminogen activator inhibitor (PAI-1) genotypes, PAI-1 levels, and their potential regulation by hypertriglyceridemic (HTG) very low density lipoprotein (VLDL) and lipoprotein(a) [Lp(a)] was examined in a PAI-1 genotyped human umbilical vein endothelial cell (HUVEC) culture model system. Individual human umbilical veins were used to obtain cultured ECs and were genotyped for PAI-1 by using the HindIII restriction fragment length polymorphism (RFLP) as a marker for genetic variation. Digested genomic DNA, examined by Southern blot analysis and probed with an [alpha-32P]dCTP-labeled 2.2-kb PAI-1 cDNA, yielded three RFLPs designated 1/1 (22-kb band only), 1/2 (22-plus 18-kb bands), and 2/2 (18-kb band only). Individual PAI-1 genotyped HUVEC cultures were incubated in the absence or presence of HTG-VLDL (0 to 50 micrograms/mL) or Lp(a) (0 to 50 micrograms/mL) at 37 degrees C for various times (4 to 24 hours), followed by analyses of PAI-1 antigen (by ELISA) and mRNA (by ribonuclease protection assay) levels, EC surface-localized plasmin generation assays, and nuclear run-on transcription assays. Secreted PAI-1 antigen levels were increased approximately 2- to 3-fold by HTG-VLDL and approximately 1.6 to 2-fold by Lp(a); mRNA levels were increased approximately 3- to 4.5-fold by HTG-VLDL and approximately 2.5- to 3.2-fold by Lp(a) compared with medium-incubated controls, primarily in the 2/2 PAI-1 genotype HUVEC cultures. Increases in PAI-1 mRNA induced by HTG-VLDL or Lp(a) could be abolished by coincubation with actinomycin D (2 x 10(-6) mol/mL) or puromycin (1 microgram/mL). In addition, nuclear transcription run-on assays typically demonstrated that HTG-VLDL increased PAI-1 gene transcription rates by approximately 5- to 6-fold and approximately 4- to 5-fold, respectively, primarily in the 2/2 PAI-1 genotype HUVEC cultures compared with 1/1 PAI-1 genotype HUVEC cultures or medium-incubated controls. The positive control interleukin-1 increased both 2/2 and 1/1 PAI-1 mRNA levels by approximately 5- to 6-fold. Increased PAI-1 antigen and mRNA expression were associated with a concomitant 50% to 60% decrease in plasmin generation. These combined results demonstrate the genotype-specific regulation of PAI-1 expression by HTG-VLDL and Lp(a) and further indicate that these risk factor-associated components regulate PAI-1 gene expression at the transcriptional level in cultured HUVECs. Results from these studies further suggest that individuals with this responsive 2/2 PAI-1 genotype may reflect the additional inherent potential for later HTG-VLDL- or Lp(a)-induced fibrinolytic dysfunction, resulting in the early initiation of thrombosis, atherogenesis, and coronary artery disease. | lld:pubmed |
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| pubmed-article:9409314 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9409314 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9409314 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9409314 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9409314 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9409314 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9409314 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9409314 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9409314 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9409314 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:9409314 | pubmed:issn | 1079-5642 | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:FlessG MGM | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:BooyseF MFM | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:GianturcoS... | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:BradleyW AWA | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:GrenettH EHE | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:BrownS LSL | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:LiX NXN | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:BenzaR LRL | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:TabengwaE MEM | lld:pubmed |
| pubmed-article:9409314 | pubmed:author | pubmed-author:DemissieSS | lld:pubmed |
| pubmed-article:9409314 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9409314 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:9409314 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9409314 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9409314 | pubmed:pagination | 3215-23 | lld:pubmed |
| pubmed-article:9409314 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:9409314 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9409314 | pubmed:articleTitle | Genotype-specific transcriptional regulation of PAI-1 expression by hypertriglyceridemic VLDL and Lp(a) in cultured human endothelial cells. | lld:pubmed |
| pubmed-article:9409314 | pubmed:affiliation | Division of Cardiovascular Disease, University of Alabama at Birmingham 35294-2170, USA. | lld:pubmed |
| pubmed-article:9409314 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9409314 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:9409314 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9409314 | lld:pubmed |
