PMID- 25441669
OWN - NLM
STAT- MEDLINE
DCOM- 20150409
LR  - 20161125
IS  - 1097-6809 (Electronic)
IS  - 0741-5214 (Linking)
VI  - 61
IP  - 2
DP  - 2015 Feb
TI  - Identification of a potential proinflammatory genetic profile influencing carotid 
      plaque vulnerability.
PG  - 374-81
LID - S0741-5214(14)01681-4 [pii]
LID - 10.1016/j.jvs.2014.08.113 [doi]
AB  - OBJECTIVE: Atherosclerosis and vascular remodeling after injury are driven by 
      inflammation and mononuclear cell infiltration. Unstable atherosclerotic plaques 
      are characterized by a large necrotic core. In this study we investigated the 
      distribution and interaction between gene polymorphisms encoding proinflammatory 
      molecules in an Italian population with internal carotid artery stenosis (ICAS). 
      We also evaluated whether reciprocal interaction between these gene polymorphisms 
      increased the risk of plaque vulnerability. METHODS: In this genetic association 
      study, 11 proinflammatory gene polymorphisms were analyzed in 933 individuals 
      comprising 344 patients with ICAS who underwent carotid endarterectomy and 589 
      controls without ultrasound evidence of atherosclerosis or intimal thickening. 
      RESULTS: We found that interleukin (IL) 6 (IL-6), IL-1beta, monocyte chemoattractant 
      protein-1 (CCL2) macrophage inflammatory protein-1alpha (CCL3), E-selectin (SELE), 
      intercellular adhesion molecule 1 (ICAM1), and matrix metalloproteinase-3 
      (MMP-3), and 9 (MMP-9) gene variants were independently and significantly 
      associated with ICAS. The association remained significant even after the 
      Bonferroni correction. We also found a genetic profile associated with different 
      risks for ICAS, depending on the number of high-risk genotypes simultaneously 
      present in an individual. Furthermore, proinflammatory genetic profiles are 
      significantly more common in individuals with unstable carotid plaque. 
      CONCLUSIONS: Our study shows, for the first time, a reciprocal interaction 
      between proinflammatory genotypes for the development and progression of ICAS.
CI  - Copyright (c) 2015 Society for Vascular Surgery. Published by Elsevier Inc. All 
      rights reserved.
FAU - Biscetti, Federico
AU  - Biscetti F
AD  - Department of Medicine, A. Gemelli University Hospital, Catholic University 
      School of Medicine, Rome, Italy; Laboratory of Vascular Biology and Genetics, 
      Catholic University School of Medicine, Rome, Italy.
FAU - Straface, Giuseppe
AU  - Straface G
AD  - Department of Medicine, St M. Goretti Hospital, Latina, Italy.
FAU - Bertoletti, Giovanni
AU  - Bertoletti G
AD  - Department of Vascular Surgery, St M. Goretti Hospital, Latina, Italy.
FAU - Vincenzoni, Claudio
AU  - Vincenzoni C
AD  - Department of Vascular Surgery, A. Gemelli University Hospital, Catholic 
      University School of Medicine, Rome, Italy.
FAU - Snider, Francesco
AU  - Snider F
AD  - Department of Vascular Surgery, A. Gemelli University Hospital, Catholic 
      University School of Medicine, Rome, Italy.
FAU - Arena, Vincenzo
AU  - Arena V
AD  - Department of Pathology, Catholic University School of Medicine, Rome, Italy.
FAU - Landolfi, Raffaele
AU  - Landolfi R
AD  - Department of Medicine, A. Gemelli University Hospital, Catholic University 
      School of Medicine, Rome, Italy.
FAU - Flex, Andrea
AU  - Flex A
AD  - Department of Medicine, A. Gemelli University Hospital, Catholic University 
      School of Medicine, Rome, Italy; Laboratory of Vascular Biology and Genetics, 
      Catholic University School of Medicine, Rome, Italy. Electronic address: 
      andrea.flex@rm.unicatt.it.
LA  - eng
PT  - Journal Article
DEP - 20141031
PL  - United States
TA  - J Vasc Surg
JT  - Journal of vascular surgery
JID - 8407742
RN  - 0 (Genetic Markers)
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Aged
MH  - Carotid Artery, Internal/diagnostic imaging/*pathology/surgery
MH  - Carotid Intima-Media Thickness
MH  - Carotid Stenosis/diagnosis/*genetics/immunology/surgery
MH  - Case-Control Studies
MH  - Disease Progression
MH  - Endarterectomy, Carotid
MH  - Female
MH  - Gene Frequency
MH  - Genetic Association Studies
MH  - Genetic Markers
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Inflammation/diagnostic imaging/*genetics/immunology
MH  - *Inflammation Mediators
MH  - Italy
MH  - Male
MH  - Phenotype
MH  - *Plaque, Atherosclerotic
MH  - *Polymorphism, Single Nucleotide
MH  - Predictive Value of Tests
MH  - Risk Factors
MH  - Rupture, Spontaneous
EDAT- 2014/12/03 06:00
MHDA- 2015/04/10 06:00
CRDT- 2014/12/03 06:00
PHST- 2014/04/14 00:00 [received]
PHST- 2014/08/28 00:00 [accepted]
PHST- 2014/12/03 06:00 [entrez]
PHST- 2014/12/03 06:00 [pubmed]
PHST- 2015/04/10 06:00 [medline]
AID - S0741-5214(14)01681-4 [pii]
AID - 10.1016/j.jvs.2014.08.113 [doi]
PST - ppublish
SO  - J Vasc Surg. 2015 Feb;61(2):374-81. doi: 10.1016/j.jvs.2014.08.113. Epub 2014 Oct 
      31.