Abstract
Inflammatory markers have consistently been associated with vascular disease. Evidence of genetic polymorphisms in inflammatory loci that predict severe carotid artery disease (CAAD) would suggest that this relationship is not secondary to other correlated factors, but related to inflammation itself. We examined the full common genetic variation in 42 inflammatory loci for prediction of severe CAAD versus ultrasound proven controls using a tagSNP approach. For selected loci, monocyte RNA levels were contrasted in subjects with and without CAAD. We confirm the association of IL6-174, FGB-455, and ALOX5 with CAAD and show that multiple ALOX5 SNPs independently predict CAAD. We provide evidence for previously unreported associations of SNPs in IL4R, NFKBIA, and PLG with CAAD, and weaker evidence for associations with CSF3, IL10RA, and VCAM1. The NFKBIA and IL10RA expression levels significantly differed between subjects with CAAD and controls. These results support a role for genetic variation related to inflammation in CAAD and a causal role for specific gene products.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 65-75 |
| Number of pages | 11 |
| Journal | Human Genetics |
| Volume | 121 |
| Issue number | 1 |
| DOIs | |
| State | Published - Mar 1 2007 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Genetics
- Genetics(clinical)
Cite this
TagSNP evaluation for the association of 42 inflammation loci and vascular disease : Evidence of IL6, FGB, ALOX5, NFKBIA, and IL4R loci effects. / Carlson, Christopher S.; Heagerty, Patrick J.; Nord, Alexander; Pritchard, David K.; Ranchalis, Jane; Boguch, Joshua M.; Duan, Hangjun; Hatsukami, Thomas S.; Schwartz, Stephen M.; Rieder, Mark J.; Nickerson, Deborah A.; Jarvik, Gail P.
In: Human Genetics, Vol. 121, No. 1, 01.03.2007, p. 65-75.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - TagSNP evaluation for the association of 42 inflammation loci and vascular disease
T2 - Evidence of IL6, FGB, ALOX5, NFKBIA, and IL4R loci effects
AU - Carlson, Christopher S.
AU - Heagerty, Patrick J.
AU - Nord, Alexander
AU - Pritchard, David K.
AU - Ranchalis, Jane
AU - Boguch, Joshua M.
AU - Duan, Hangjun
AU - Hatsukami, Thomas S.
AU - Schwartz, Stephen M.
AU - Rieder, Mark J.
AU - Nickerson, Deborah A.
AU - Jarvik, Gail P.
PY - 2007/3/1
Y1 - 2007/3/1
N2 - Inflammatory markers have consistently been associated with vascular disease. Evidence of genetic polymorphisms in inflammatory loci that predict severe carotid artery disease (CAAD) would suggest that this relationship is not secondary to other correlated factors, but related to inflammation itself. We examined the full common genetic variation in 42 inflammatory loci for prediction of severe CAAD versus ultrasound proven controls using a tagSNP approach. For selected loci, monocyte RNA levels were contrasted in subjects with and without CAAD. We confirm the association of IL6-174, FGB-455, and ALOX5 with CAAD and show that multiple ALOX5 SNPs independently predict CAAD. We provide evidence for previously unreported associations of SNPs in IL4R, NFKBIA, and PLG with CAAD, and weaker evidence for associations with CSF3, IL10RA, and VCAM1. The NFKBIA and IL10RA expression levels significantly differed between subjects with CAAD and controls. These results support a role for genetic variation related to inflammation in CAAD and a causal role for specific gene products.
AB - Inflammatory markers have consistently been associated with vascular disease. Evidence of genetic polymorphisms in inflammatory loci that predict severe carotid artery disease (CAAD) would suggest that this relationship is not secondary to other correlated factors, but related to inflammation itself. We examined the full common genetic variation in 42 inflammatory loci for prediction of severe CAAD versus ultrasound proven controls using a tagSNP approach. For selected loci, monocyte RNA levels were contrasted in subjects with and without CAAD. We confirm the association of IL6-174, FGB-455, and ALOX5 with CAAD and show that multiple ALOX5 SNPs independently predict CAAD. We provide evidence for previously unreported associations of SNPs in IL4R, NFKBIA, and PLG with CAAD, and weaker evidence for associations with CSF3, IL10RA, and VCAM1. The NFKBIA and IL10RA expression levels significantly differed between subjects with CAAD and controls. These results support a role for genetic variation related to inflammation in CAAD and a causal role for specific gene products.
UR - http://www.scopus.com/inward/record.url?scp=33947241740&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33947241740&partnerID=8YFLogxK
U2 - 10.1007/s00439-006-0289-8
DO - 10.1007/s00439-006-0289-8
M3 - Article
C2 - 17115186
AN - SCOPUS:33947241740
VL - 121
SP - 65
EP - 75
JO - Human Genetics
JF - Human Genetics
SN - 0340-6717
IS - 1
ER -