Functional Genomics of the 9p21.3 Locus for Atherosclerosis: Clarity or Confusion?

The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary artery atherosclerotic disease (CAD). The 59 single nucleotide polymorphisms that show highest association with CAD are clustered in a region 1...

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Published in	Current cardiology reports Vol. 16; no. 7; p. 502
Main Authors	Chen, Hsiao-Huei, Almontashiri, Naif A. M., Antoine, Darlène, Stewart, Alexandre F. R.
Format	Journal Article
Language	English
Published	Boston Springer US 01.07.2014
Subjects	Atherosclerosis - genetics Cardiology Cardiovascular Genomics (R McPherson Chromosomes, Human, Pair 9 - genetics Genome-Wide Association Study Genomics Humans Medicine Medicine & Public Health Phenotype Section Editor Signal Transduction Topical Collection on Cardiovascular Genomics Cell proliferation Enhancers Atherosclerosis Macrophages 9p21.3 CAD risk locus Vascular smooth muscle cells Functional genomics
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Abstract	The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary artery atherosclerotic disease (CAD). The 59 single nucleotide polymorphisms that show highest association with CAD are clustered in a region 100,000 to 150,000 base pairs 5′ to the cyclin-dependent kinase inhibitors CDKN2B (coding for p15 ink4b ) and CDKN2A (coding for p16 ink4a and p14 ARF ). This region also covers the 3′ end of a long noncoding RNA transcribed antisense to CDKN2B ( CDKN2BAS , aka ANRIL for antisense noncoding RNA at the ink4 locus) whose expression has been linked to chromatin remodeling at the locus. Despite intensive investigation over the past 7 years, the functional significance of the 9p21.3 locus remains elusive. Other variants at this locus have been associated with glaucoma, glioma, and type 2 diabetes mellitus, diseases that implicate tissue-resident macrophages. Here, we review the evidence that genetic variants at 9p21.3 disrupt tissue-specific enhancers and propose new insights to guide future studies.
AbstractList	The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary artery atherosclerotic disease (CAD). The 59 single nucleotide polymorphisms that show highest association with CAD are clustered in a region 100,000 to 150,000 base pairs 5′ to the cyclin-dependent kinase inhibitors CDKN2B (coding for p15 ink4b ) and CDKN2A (coding for p16 ink4a and p14 ARF ). This region also covers the 3′ end of a long noncoding RNA transcribed antisense to CDKN2B ( CDKN2BAS , aka ANRIL for antisense noncoding RNA at the ink4 locus) whose expression has been linked to chromatin remodeling at the locus. Despite intensive investigation over the past 7 years, the functional significance of the 9p21.3 locus remains elusive. Other variants at this locus have been associated with glaucoma, glioma, and type 2 diabetes mellitus, diseases that implicate tissue-resident macrophages. Here, we review the evidence that genetic variants at 9p21.3 disrupt tissue-specific enhancers and propose new insights to guide future studies. The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary artery atherosclerotic disease (CAD). The 59 single nucleotide polymorphisms that show highest association with CAD are clustered in a region 100,000 to 150,000 base pairs 5' to the cyclin-dependent kinase inhibitors CDKN2B (coding for p15(ink4b)) and CDKN2A (coding for p16(ink4a) and p14(ARF)). This region also covers the 3' end of a long noncoding RNA transcribed antisense to CDKN2B (CDKN2BAS, aka ANRIL for antisense noncoding RNA at the ink4 locus) whose expression has been linked to chromatin remodeling at the locus. Despite intensive investigation over the past 7 years, the functional significance of the 9p21.3 locus remains elusive. Other variants at this locus have been associated with glaucoma, glioma, and type 2 diabetes mellitus, diseases that implicate tissue-resident macrophages. Here, we review the evidence that genetic variants at 9p21.3 disrupt tissue-specific enhancers and propose new insights to guide future studies.The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary artery atherosclerotic disease (CAD). The 59 single nucleotide polymorphisms that show highest association with CAD are clustered in a region 100,000 to 150,000 base pairs 5' to the cyclin-dependent kinase inhibitors CDKN2B (coding for p15(ink4b)) and CDKN2A (coding for p16(ink4a) and p14(ARF)). This region also covers the 3' end of a long noncoding RNA transcribed antisense to CDKN2B (CDKN2BAS, aka ANRIL for antisense noncoding RNA at the ink4 locus) whose expression has been linked to chromatin remodeling at the locus. Despite intensive investigation over the past 7 years, the functional significance of the 9p21.3 locus remains elusive. Other variants at this locus have been associated with glaucoma, glioma, and type 2 diabetes mellitus, diseases that implicate tissue-resident macrophages. Here, we review the evidence that genetic variants at 9p21.3 disrupt tissue-specific enhancers and propose new insights to guide future studies. The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary artery atherosclerotic disease (CAD). The 59 single nucleotide polymorphisms that show highest association with CAD are clustered in a region 100,000 to 150,000 base pairs 5' to the cyclin-dependent kinase inhibitors CDKN2B (coding for p15(ink4b)) and CDKN2A (coding for p16(ink4a) and p14(ARF)). This region also covers the 3' end of a long noncoding RNA transcribed antisense to CDKN2B (CDKN2BAS, aka ANRIL for antisense noncoding RNA at the ink4 locus) whose expression has been linked to chromatin remodeling at the locus. Despite intensive investigation over the past 7 years, the functional significance of the 9p21.3 locus remains elusive. Other variants at this locus have been associated with glaucoma, glioma, and type 2 diabetes mellitus, diseases that implicate tissue-resident macrophages. Here, we review the evidence that genetic variants at 9p21.3 disrupt tissue-specific enhancers and propose new insights to guide future studies.
ArticleNumber	502
Author	Antoine, Darlène Stewart, Alexandre F. R. Chen, Hsiao-Huei Almontashiri, Naif A. M.
Author_xml	– sequence: 1 givenname: Hsiao-Huei surname: Chen fullname: Chen, Hsiao-Huei organization: Ottawa Hospital Research Institute – sequence: 2 givenname: Naif A. M. surname: Almontashiri fullname: Almontashiri, Naif A. M. organization: John and Jennifer Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute – sequence: 3 givenname: Darlène surname: Antoine fullname: Antoine, Darlène organization: John and Jennifer Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute – sequence: 4 givenname: Alexandre F. R. surname: Stewart fullname: Stewart, Alexandre F. R. email: astewart@ottawaheart.ca organization: John and Jennifer Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute
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Keywords	Cell proliferation Enhancers Atherosclerosis Macrophages 9p21.3 CAD risk locus Vascular smooth muscle cells Functional genomics
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Snippet	The 9p21.3 locus was the first to yield to genome-wide association studies (GWAS) seeking common genetic variants predisposing to increased risk of coronary...
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SubjectTerms	Atherosclerosis - genetics Cardiology Cardiovascular Genomics (R McPherson Chromosomes, Human, Pair 9 - genetics Genome-Wide Association Study Genomics Humans Medicine Medicine & Public Health Phenotype Section Editor Signal Transduction Topical Collection on Cardiovascular Genomics
Title	Functional Genomics of the 9p21.3 Locus for Atherosclerosis: Clarity or Confusion?
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