| Genetic and clinical correlates of early-outgrowth colony-forming units. | |
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MedLine Citation:
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PMID: 21493818 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Several bone marrow-derived cell populations may have angiogenic activity, including cells termed endothelial progenitor cells. Decreased numbers of circulating angiogenic cell populations have been associated with increased cardiovascular risk. However, few data exist from large, unselected samples, and the genetic determinants of these traits are unclear. METHODS AND RESULTS: We examined the clinical and genetic correlates of early-outgrowth colony-forming units (CFUs) in 1799 participants of the Framingham Heart Study (mean age, 66 years; 54% women). Among individuals without cardiovascular disease (n = 1612), CFU number was inversely related to advanced age (P = 0.004), female sex (P = 0.04), and triglycerides (P = 0.008) and positively related to hormone replacement (P = 0.008) and statin therapy (P = 0.027) in stepwise multivariable analyses. Overall, CFU number was inversely related to the Framingham risk score (P = 0.01) but not with prevalent cardiovascular disease. In genome-wide association analyses in the entire sample, polymorphisms were associated with CFUs at the MOSC1 locus (P = 3.3 × 10(-7)) and at the SLC22A3-LPAL2-LPA locus (P = 4.9 × 10(-7)), a previously replicated susceptibility locus for myocardial infarction. Furthermore, alleles at the SLC22A3-LPAL2-LPA locus that were associated with decreased CFUs were also related to increased risk of myocardial infarction (P = 1.1 × 10(-4)). CONCLUSIONS: In a community-based sample, early-outgrowth CFUs are inversely associated with select cardiovascular risk factors. Furthermore, genetic variants at the SLC22A3-LPAL2-LPA locus are associated with both decreased CFUs and an increased risk of myocardial infarction. These findings are consistent with the hypothesis that decreased circulating angiogenic cell populations promote susceptibility to myocardial infarction. |
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Authors:
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Stanley Y Shaw; Susan Cheng; L Adrienne Cupples; Martin G Larson; Elizabeth L McCabe; Julius S Ngwa; Ying A Wang; Roderick P Martin; Rachael J Klein; Basma Hashmi; Olujimi A Ajijola; Evan Lau; Christopher J O'Donnell; Ramachandran S Vasan; Kenneth S Cohen; Thomas J Wang |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-04-14 |
Journal Detail:
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Title: Circulation. Cardiovascular genetics Volume: 4 ISSN: 1942-3268 ISO Abbreviation: Circ Cardiovasc Genet Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-06-15 Completed Date: 2011-09-30 Revised Date: 2013-03-04 |
Medline Journal Info:
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Nlm Unique ID: 101489144 Medline TA: Circ Cardiovasc Genet Country: United States |
Other Details:
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Languages: eng Pagination: 296-304 Citation Subset: IM |
Affiliation:
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Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aged Bone Marrow Cells* / cytology, physiology Cardiovascular Diseases / physiopathology* Endothelial Cells* / cytology, physiology Female Humans Male Middle Aged Polymorphism, Single Nucleotide Risk Factors Stem Cells* / cytology, physiology |
| Grant Support | |
ID/Acronym/Agency:
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N01 HC025195/HC/NHLBI NIH HHS; N01-HC-25195/HC/NHLBI NIH HHS; R01 HL083197-04/HL/NHLBI NIH HHS; R01 HL093328/HL/NHLBI NIH HHS; R01 HL093328-04/HL/NHLBI NIH HHS; R01-HL083197/HL/NHLBI NIH HHS; R01-HL93328/HL/NHLBI NIH HHS |
| Comments/Corrections | |
Comment In:
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Circ Cardiovasc Genet. 2011 Jun;4(3):218-20
[PMID:
21673309
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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