PMID- 23161441
OWN - NLM
STAT- MEDLINE
DCOM- 20131029
LR  - 20220409
IS  - 1432-5233 (Electronic)
IS  - 0940-5429 (Print)
IS  - 0940-5429 (Linking)
VI  - 50
IP  - 3
DP  - 2013 Jun
TI  - Polymorphisms in the Selenoprotein S gene and subclinical cardiovascular disease 
      in the Diabetes Heart Study.
PG  - 391-9
LID - 10.1007/s00592-012-0440-z [doi]
AB  - Selenoprotein S (SelS) has previously been associated with a range of 
      inflammatory markers, particularly in the context of cardiovascular disease 
      (CVD). The aim of this study was to examine the role of SELS genetic variants in 
      risk for subclinical CVD and mortality in individuals with type 2 diabetes 
      mellitus (T2DM). The association between 10 polymorphisms tagging SELS and 
      coronary (CAC), carotid (CarCP) and abdominal aortic calcified plaque, carotid 
      intima media thickness and other known CVD risk factors was examined in 1220 
      European Americans from the family-based Diabetes Heart Study. The strongest 
      evidence of association for SELS SNPs was observed for CarCP; rs28665122 (5' 
      region; beta = 0.329, p = 0.044), rs4965814 (intron 5; beta = 0.329, p = 0.036), 
      rs28628459 (3' region; beta = 0.331, p = 0.039) and rs7178239 (downstream; beta = 
      0.375, p = 0.016) were all associated. In addition, rs12917258 (intron 5) was 
      associated with CAC (beta = -0.230, p = 0.032), and rs4965814, rs28628459 and 
      rs9806366 were all associated with self-reported history of prior CVD (p = 
      0.020-0.043). These results suggest a potential role for the SELS region in the 
      development subclinical CVD in this sample enriched for T2DM. Further 
      understanding the mechanisms underpinning these relationships may prove important 
      in predicting and managing CVD complications in T2DM.
FAU - Cox, Amanda J
AU  - Cox AJ
AD  - Center for Human Genomics, Wake Forest School of Medicine, Winston-Salem, NC, 
      USA.
FAU - Lehtinen, Allison B
AU  - Lehtinen AB
FAU - Xu, Jianzhao
AU  - Xu J
FAU - Langefeld, Carl D
AU  - Langefeld CD
FAU - Freedman, Barry I
AU  - Freedman BI
FAU - Carr, J Jeffrey
AU  - Carr JJ
FAU - Bowden, Donald W
AU  - Bowden DW
LA  - eng
GR  - R01 HL67348/HL/NHLBI NIH HHS/United States
GR  - R01 NS058700/NS/NINDS NIH HHS/United States
GR  - R01 HL067348/HL/NHLBI NIH HHS/United States
GR  - R01 HL09230/HL/NHLBI NIH HHS/United States
GR  - R01 HL092301/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20121116
PL  - Germany
TA  - Acta Diabetol
JT  - Acta diabetologica
JID - 9200299
RN  - 0 (Membrane Proteins)
RN  - 0 (SELENOS protein, human)
RN  - 0 (Selenoproteins)
SB  - IM
MH  - Aged
MH  - Cardiovascular Diseases/epidemiology/*genetics
MH  - Carotid Artery Diseases/epidemiology/genetics
MH  - Carotid Intima-Media Thickness
MH  - Diabetes Mellitus, Type 2/epidemiology/*genetics
MH  - Diabetic Angiopathies/epidemiology/genetics
MH  - Female
MH  - Genotype
MH  - Humans
MH  - Introns/genetics
MH  - Linkage Disequilibrium
MH  - Male
MH  - Membrane Proteins/*genetics
MH  - Middle Aged
MH  - Polymorphism, Single Nucleotide
MH  - Risk Factors
MH  - Selenoproteins/*genetics
MH  - Vascular Calcification/epidemiology/genetics
PMC - PMC3597768
MID - NIHMS423437
COIS- CONFLICT OF INTEREST: None
EDAT- 2012/11/20 06:00
MHDA- 2013/10/30 06:00
PMCR- 2014/06/01
CRDT- 2012/11/20 06:00
PHST- 2012/07/24 00:00 [received]
PHST- 2012/11/03 00:00 [accepted]
PHST- 2012/11/20 06:00 [entrez]
PHST- 2012/11/20 06:00 [pubmed]
PHST- 2013/10/30 06:00 [medline]
PHST- 2014/06/01 00:00 [pmc-release]
AID - 10.1007/s00592-012-0440-z [doi]
PST - ppublish
SO  - Acta Diabetol. 2013 Jun;50(3):391-9. doi: 10.1007/s00592-012-0440-z. Epub 2012 
      Nov 16.