PMID- 12732396
OWN - NLM
STAT- MEDLINE
DCOM- 20031211
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 168
IP  - 1
DP  - 2003 May
TI  - A novel functional polymorphism in the PECAM-1 gene (53G>A) is associated with 
      progression of atherosclerosis in the LOCAT and REGRESS studies.
PG  - 131-8
AB  - A 53G>A polymorphism identified in the 5' untranslated region (5'UTR) of the 
      platelet endothelial cell adhesion molecule-1 (PECAM-1) gene alters a putative 
      shear stress responsive element (SSRE). PECAM-1 was shown to be responsive to 
      shear stress and transient transfection of human umbilical vein endothelial cell 
      (HUVECs) with two luciferase reporter constructs driven by the PECAM-1 promoter 
      and 5'UTR showed a response of the 53G allele, not the 53A allele, to shear 
      stress. Association between the 53G>A, and the previously published L125V 
      polymorphism, and coronary atherosclerosis was examined in two angiographic 
      studies. The frequencies of the rare alleles of the 53G>A and L125V polymorphisms 
      were 0.01 and 0.49, respectively, in the Lopid Coronary Angiography Trial (LOCAT) 
      study and 0.02 and 0.49, respectively, in the Regression Growth Evaluation Statin 
      Study (REGRESS) study. Compared with 53G homozygotes, carriers of the 53A allele 
      showed less focal progression of disease in the LOCAT study and a similar trend 
      in the diffuse progression of disease in the REGRESS study, whereas no 
      association between L125V and coronary atherosclerosis was observed in either 
      study. These data demonstrate that the PECAM-1 gene is responsive to shear stress 
      in vitro and that decreased PECAM-1 gene expression in 53A carriers may influence 
      reduced progression of vessel stenosis in patients with coronary artery disease.
FAU - Elrayess, Mohamed A
AU  - Elrayess MA
AD  - The Centre for Cardiovascular Genetics, British Heart Foundation Laboratories, 
      Royal Free and University College Medical School, University College London, 
      Rayne Building, 5 University Street, UK. m.rayess@ucl.ac.uk
FAU - Webb, Karen E
AU  - Webb KE
FAU - Flavell, David M
AU  - Flavell DM
FAU - Syvanne, Mikko
AU  - Syvanne M
FAU - Taskinen, Marja-Riitta
AU  - Taskinen MR
FAU - Frick, M Heikki
AU  - Frick MH
FAU - Nieminen, Markku S
AU  - Nieminen MS
FAU - Kesaniemi, Y Antero
AU  - Kesaniemi YA
FAU - Pasternack, Amos
AU  - Pasternack A
FAU - Jukema, J Wouter
AU  - Jukema JW
FAU - Kastelein, John J P
AU  - Kastelein JJ
FAU - Zwinderman, Aeilko H
AU  - Zwinderman AH
FAU - Humphries, Steve E
AU  - Humphries SE
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (DNA, Complementary)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Platelet Endothelial Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases)
SB  - IM
MH  - Aged
MH  - Alleles
MH  - Computer Systems
MH  - Coronary Angiography
MH  - Coronary Artery Disease/drug therapy/*genetics
MH  - DNA, Complementary/genetics
MH  - Disease Progression
MH  - Endothelium, Vascular/chemistry/cytology
MH  - Finland
MH  - Follow-Up Studies
MH  - Gene Frequency/genetics
MH  - Gene Order/*genetics
MH  - Genetic Predisposition to Disease/genetics
MH  - Genotype
MH  - Glyceraldehyde-3-Phosphate Dehydrogenases/genetics
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - Intercellular Adhesion Molecule-1/genetics
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Platelet Endothelial Cell Adhesion Molecule-1/*genetics
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Genetic/*genetics
MH  - Promoter Regions, Genetic/genetics
MH  - Statistics as Topic
MH  - Stress, Mechanical
MH  - Transfection
MH  - Umbilical Veins/chemistry/cytology
EDAT- 2003/05/07 05:00
MHDA- 2003/12/12 05:00
CRDT- 2003/05/07 05:00
PHST- 2003/05/07 05:00 [pubmed]
PHST- 2003/12/12 05:00 [medline]
PHST- 2003/05/07 05:00 [entrez]
AID - S0021-9150(03)00089-3 [pii]
AID - 10.1016/s0021-9150(03)00089-3 [doi]
PST - ppublish
SO  - Atherosclerosis. 2003 May;168(1):131-8. doi: 10.1016/s0021-9150(03)00089-3.