共查询到20条相似文献,搜索用时 15 毫秒
1.
Chemokines regulates the trafficking of leukocytes to the site of inflammation hence may be implicated in cardiac events.
Currently no consistent effects have been revealed their role in acute myocardial infarction (MI). The aim of current study
was to investigate the impact of human chemokine receptor genetic variants, CCR5-Δ32 insertion/deletion, CCR5-59029-A/G, CX3CR1-V249I
and CX3CR1-T280 M on acute MI. 230 acute MI and 300 controls were examined. Patients carrying CCR5-Δ32 genotype were at three
times higher risk of developing MI odds ratio (OR, 3.24, CI 1.127–9.356, P = 0.04). Significant association was found with risk of acute MI in recipients who possessed homozygous 59029-A allele (OR
1.47, CI 1.03–2.09, P = 0.03). While CX3CR1-I249 and M280 were found to be protective in MI patients with OR 0.46, CI 0.32–0.66, P < 0.0001 and OR 0.36, CI 0.24–0.55, P < 0.0001, respectively. It might be possible that risk of acute MI is associated with genetic variation in chemokine receptors,
i.e., CCR5 and CX3CR1. 相似文献
2.
Alan Lopez-Lopez Josep Gamez Emilio Syriani Miguel Morales Maria Salvado Manuel J. Rodríguez Nicole Mahy Jose M. Vidal-Taboada 《PloS one》2014,9(5)
The objective of this study was to investigate the association of functional variants of the human CX3CR1 gene (Fractalkine receptor) with the risk of Amyotrophic Lateral Sclerosis (ALS), the survival and the progression rate of the disease symptoms in a Spanish ALS cohort. 187 ALS patients (142 sporadic [sALS] and 45 familial) and 378 controls were recruited. We investigated CX3CR1 V249I (rs3732379) and T280M (rs3732378) genotypes and their haplotypes as predictors of survival, the progression rate of the symptoms (as measured by ALSFRS-R and FVC decline) and the risk of suffering ALS disease. The results indicated that sALS patients with CX3CR1 249I/I or 249V/I genotypes presented a shorter survival time (42.27±4.90) than patients with 249V/V genotype (67.65±7.42; diff −25.49 months 95%CI [−42.79,−8.18]; p = 0.004; adj-p = 0.018). The survival time was shorter in sALS patients with spinal topography and CX3CR1 249I alleles (diff = −29.78 months; 95%CI [−49.42,−10.14]; p = 0.003). The same effects were also observed in the spinal sALS patients with 249I–280M haplotype (diff = −27.02 months; 95%CI [−49.57, −4.48]; p = 0.019). In the sALS group, the CX3CR1 249I variant was associated with a faster progression of the disease symptoms (OR = 2.58; 95IC% [1.32, 5.07]; p = 0.006; adj-p = 0.027). There was no evidence for association of these two CX3CR1 variants with ALS disease risk. The association evidenced herein is clinically relevant and indicates that CX3CR1 could be a disease-modifying gene in sALS. The progression rate of the disease''s symptoms and the survival time is affected in patients with one or two copies of the CX3CR1 249I allele. The CX3CR1 is the most potent ALS survival genetic factor reported to date. These results reinforce the role of the immune system in ALS pathogenesis. 相似文献
3.
Dave Sirois‐Gagnon Annie Chamberland Stéphanie Perron Diane Brisson Daniel Gaudet Catherine Laprise 《Obesity (Silver Spring, Md.)》2011,19(1):222-227
The inflammatory component in obesity is now well established. The CX3CR1 gene encodes the fractalkine (CX3CL1) receptor and has two coding single‐nucleotide polymorphisms, V249I and T280M, linked to a lower risk of other inflammatory diseases such as coronary artery disease (CAD) and asthma. To determine whether CX3CR1 is associated with obesity, we genotyped the V249I and T280M polymorphisms of the CX3CR1 gene in subjects with a BMI ≥30 kg/m2 and nonobese controls with a BMI <30 kg/m2. Binary logistic regression analyses revealed that the 280MM genotype was associated with obesity (P = 0.022). A gender‐specific one‐way ANOVA was also conducted to investigate mean BMI and waist circumference differences between genotypes of each polymorphism. For both polymorphisms independently, women carrying two copies of the minor allele had significant higher mean waist circumference than those carrying only one copy of the minor allele (MM > TM, P = 0.031; II > VI, P = 0.013) or those who were homozygous for the major allele (MM > TT, P = 0.005; II > VV, P = 0.006). We also observed significant higher mean waist circumference in men carrying one copy of the minor allele when compared to those who were homozygous for the major allele for the T280M polymorphism (TM > TT, P = 0.029). This study suggests that CX3CR1, a biomarker of obesity in this sample, constitutes a potential target for further investigation of the role of inflammation in the expression of obesity‐related phenotypes. 相似文献
4.
Alain Stepanian Soraya Benchenni Tiphaine Beillat-Lucas Sophie Omnes Fannie Defay Edith Peynaud-Debayle Gabriel Baron Agnès Le Querrec Michel Dreyfus Laurence Salomon Vassilis Tsatsaris Dominique de Prost Laurent Mandelbrot for the ECLAXIR study group 《PloS one》2009,4(7)
Background
Preeclampsia and coronary-artery disease share risk factors, suggesting common pathophysiological mechanisms. CX3CR1/CX3CL1 mediates leukocyte migration and adhesion and has been implicated in the pathophysiology of several inflammatory diseases. M280/I249 variants of CX3CR1 are associated with an atheroprotective effect and reduced endothelial dysfunction. The aim of this study was to search for an association between V249I and T280M polymorphisms of CX3CR1, preeclampsia and endothelial dysfunction.Methodology/Principal Findings
We explored these polymorphisms with real-time polymerase chain reaction in a case-control study (184 white women with preeclampsia and 184 matched normotensive pregnant women). Endothelial dysfunction biomarkers including von Willebrand factor, VCAM-1 and thrombomodulin, as well as the soluble form of CX3CL1 were measured by enzyme-linked immunosorbent assays (ELISA). The I249 and M280 alleles were associated neither with preeclampsia, nor with its more severe form or with endothelial injury. In contrast, we found a trend toward increased CX3CL1 levels in preeclampsia patients, especially in early-onset- preeclampsia as compared to its level in later-onset- preeclampsia.Conclusions/Significance
This is the first study to characterize the CX3CR1 gene polymorphisms in patients with preeclampsia. We found no differences in genotype or haplotype frequencies between patients with PE and normal pregnancies, suggesting that maternal CX3CR1 V249I and T280M polymorphisms do not increase susceptibility to preeclampsia. Further studies should be performed to directly evaluate the pathophysiological role of CX3CL1, a molecule abundantly expressed in endometrium, which has been shown to stimulate human trophoblast migration. 相似文献5.
6.
Nadif R Mintz M Rivas-Fuentes S Jedlicka A Lavergne E Rodero M Kauffmann F Combadière C Kleeberger SR 《Cytokine》2006,33(3):171-178
Chemokines and their receptors are key regulators of inflammation and may participate in the lung fibrotic process. Associations of polymorphisms in CCL5 (G-403A) and its receptor CCR5 (Delta32), CCL2 (A-2578G) and CCR2 (V64I), and CX3CR1 V249I and T280M with coal worker's pneumoconiosis (CWP) were investigated in 209 miners examined in 1990, 1994 and 1999. Coal dust exposure was assessed by job history and ambient measures. The main health outcome was lung computed tomography (CT) score in 1990. Internal coherence was assessed by studying CT score in 1994, 4-year change in CT score, and CWP prevalence in 1999. CCR5 Delta32 carriers had significantly higher CT score in 1990 and 1994 (2.15 vs. 1.28, p=0.01; 3.04 vs. 1.80, p=0.04). The CX3CR1 I249 allele was significantly associated with lower 1990 CT score and lower progression in 4-year change in CT score in CCR5 Delta32 carriers only (p for interaction=0.03 and 0.02). CX3CR1 V249I was associated with lower 1999 CWP prevalence (16.7%, 13.2%, 0.0% for VV, VI and II); the effect was most evident in miners with high dust exposure (31.6%, 21.7%, 0.0%). Our findings indicate that chemokine receptors CCR5 and CX3CR1 may be involved in the development of pneumoconiosis. 相似文献
7.
Daoudi M Lavergne E Garin A Tarantino N Debré P Pincet F Combadière C Deterre P 《The Journal of biological chemistry》2004,279(19):19649-19657
It was recently shown that individuals carrying the naturally occurring mutant CX3CR1-Ile(249)-Met(280) (hereafter called CX3CR1-IM) have a lower risk of cardiovascular disease than individuals homozygous for the wild-type CX3CR1-Val(249)-Thr(280) (CX3CR1-VT). We report here that peripheral blood mononuclear cells (PBMC) from individuals with the CX3CR1-IM haplotype adhered more potently to membrane-bound CX3CL1 than did PBMC from homozygous CX3CR1-VT donors. Similar excess adhesion was observed with CX3CR1-IM-transfected human embryonic kidney (HEK) cell lines tested with two different methods: the parallel plate laminar flow chamber and the dual pipette aspiration technique. Suppression of the extra adhesion in the presence of pertussis toxin indicates that G-protein mediated the underlying transduction pathway, in contrast to the G-protein-independent adhesion previously described for CX3CR1-VT. Surprisingly, HEK and PBMC that expressed CX3CR1-IM and -VT were indistinguishable when tested with the soluble form of CX3CL1 for chemotaxis, calcium release, and binding capacity. In conclusion, only the membrane-anchored form of CX3CL1 functionally discriminated between these two allelic isoforms of CX3CR1. These results suggest that each form of this ligand may lead to a different signaling pathway. The extra adhesion of CX3CR1-IM may be related to immune defenses and to atherogenesis, both of which depend substantially on adhesive intercellular events. 相似文献
8.
Vaisi-Raygani A Rahimi Z Tavilani H Vaisi-Raygani H Kiani A Aminian M Shakiba E Shakiba Y Pourmotabbed T 《Molecular biology reports》2012,39(3):2723-2731
We have previously shown that angiotensin-converting enzyme (ACE) gene D allele is an independent risk factor for early onset
coronary artery disease (CAD). Little is known about the concomitant presence of the ACE gene D allele and paraoxonase (PON1)
codon 192 arginine (Arg) on the severity of CAD. Regarding the high rate of CAD among Iranians the aim of present study was
to examine the hypothesis of synergistic effects between ACE-D and PON1-Arg alleles on predisposition and the severity of
CAD in our population. The PON1 192 and ACE insertion/deletion (I/D) genotypes were detected by PCR-RFLP and PCR, respectively
in 414 individuals undergoing their first coronary angiography. Patients were placed into one of two groups: CAD and control
without CAD or diabetes. We mentioned the synergistic effects of both genes and not ACE gene alone is a risk factor for CAD.
We found that PON1 Arg 192 and ACE D allele act synergistically to increase the risk of CAD (OR 1.3, P = 0.044). Our results showed a significant correlation between the possession of both PON1 192 Arg and the ACE D allele and
the extent of CAD in CAD patients and CAD subjects without diabetes, represented by the increased frequency of three-vessel
disease with OR 2.7, P = 0.046; χ2 = 4, P = 0.046 and OR 2.4, P = 0.051; χ2 = 3.8, P = 0.051, respectively. We found that PON1 Arg 192 and ACE D alleles act synergistically to increase the risk of CAD in CAD
patients and CAD subjects without diabetes from west of Iran, who have high frequency of three-vessel disease. Our data suggest
that PON1 192 Arg and the ACE D allele in combination with each other can be important independent risk factor for severity
of CAD in patients carrying both PON1 192 Arg and the ACE D allele in a west population of Iran. 相似文献
9.
Context
Recurrent miscarriage (RM), defined as three or more consecutive losses before the 20th week of gestation, affects 0.5–2% of pregnant women. In over 80% of cases, RM remains unexplained after investigations, suggesting the involvement of genetic factors.Objectives
The present study investigates the common polymorphisms of chemokine receptors CCR5 (NG_012637.1:g.5303A>G) and CX3CR1 (NG_016362.1:g.21065C>T, Thr280Met and NG_016362.1:g.20971G>A, Val249Ile) and their association with recurrent miscarriages (RM) among north Indian women.Participants and Methods
In a retrospective case-control study 200 well characterized patients with unexplained RM and 300 controls were genotyped for three polymorphic markers of CCR5 and CX3CR1 by restriction digestion of PCR amplified fragments.Results
Alleles and genotypes of CX3CR1 Val249Ile revealed statistically significant associations with RM cases when compared with the controls. The homozygous variant genotype Ile/Ile was found to be significantly higher among patients (p = 0.0002) when compared with the homozygous wild type Val/Val genotype. The haplotype of CX3CR1 that carried major alleles of Thr280Met and Val249Ile (T-V) showed statistically significant protective association (p < 0.0001, OR = 0.41, 95% CI = 0.31–0.54). The haplotype A-T-V (all wild type alleles) revealed a statistically significant protective association (p < 0.0001, OR = 0.41, 95% CI = 0.34–0.62), whereas the haplotypes G-T-I, A-T-I and A-M-V modified the risk of RM 1.9-fold, 5.5-fold and 5.1-fold respectively.Conclusions
A common polymorphism of CX3CR1 gene, Val240Ile is associated with the risk of RM in north Indian women. Risk of RM may also be modified by the presence of haplotypes T-I, M-V, G-T-I, A-T-I and A-M-V. 相似文献10.
Jiann-Jou Yang Wen-Hung Wang Yen-Chun Lin Hsu-Huei Weng Jen-Tsung Yang Chung-Feng Hwang Che-Min Wu Shuan-Yow Li 《Human genetics》2010,128(3):303-313
The crucial role of gap junctions, which are composed of connexin (CX) protein, in auditory functions has been confirmed by
numerous studies. In this study, we investigate the prevalence and phenotype/genotype correlation of connexin (CX) gene family
variants in a cohort of children with nonsyndromic hearing loss (HL). A total of 253 unrelated children with nonsyndromic
HL were screened for the presence of variants in 6 genes of the CX gene family. The prevalence of CX gene variants in 253
patients was 19.7% (50/253). We found the frequency of a sloping audiometric configuration was significantly higher for children
with GJB2 and GJB3 variants than for those with GJB4 and GJC3 variants (Adjusted OR = 4.89, p < 0.001). Conversely, the frequency of a flat audiometric configuration was significantly higher for children with GJB4 and GJC3 variants than for those with GJB2 and GJB3 variants (adjusted OR = 7.76, p < 0.001). The relative frequencies of multiplex families was significantly higher for children with GJB3 variants than for those with GJB2, GJB4, and GJC3 variants (Adjusted OR = 11.33, p = 0.003). Our results suggest the variants of GJC3, GJB4, and GJB3 may be the common genetic risk factor, after variants of GJB2, for the development of nonsyndromic HL in Taiwan. These data can be effectively applied to direct the clinical evaluation
of children with CX gene variants. 相似文献
11.
Pasalić D Marinković N Grsković B Ferencak G Bernat R Stavljenić-Rukavina A 《Molecular biology reports》2009,36(4):775-780
Human C-reactive protein (CRP) is a reactant involved in the acute phase response and one of the many molecular factors involved
in pathogenesis of coronary artery disease (CAD). CRP gene variants potentially mediate CRP plasma concentrations and the
development of CAD. 220 Croatian subjects with angiographically confirmed CAD and 132 control subjects were included in the
study. CRP gene polymorphisms 1059G/C and -717G/A were determined by RFLPs, using MaeIII and KspI endonuclease, respectively. Plasma concentrations of CRP and homocysteine were determined by immunoturbidimetry and FPIA,
respectively. CRP 1059G/C gene variants were significantly associated with CAD (OR = 0.50; 95% CI = 0.27, 0.94; P = 0.032). Wild GG genotype and rare allele C carrier genotypes were 184 and 22 in CAD(+) group, and 101 and 24 in CAD(−)
group, respectively. Multivariate analysis with age, gender, BMI, smoking status, hypertension and diabetes as covariates
showed that 1059C carriers had lower CRP concentrations in CAD(−) (P = 0.010) and CAD(+) subjects (P = 0.028). This allele was also significantly associated with lower plasma homocysteine concentrations in both groups (P = 0.018 for CAD(−) and 0.002 for CAD(+). There was no significant difference between CAD(+) and CAD(−) subjects in absolute
frequencies for CRP -717A/G gene variant, but multivariate analysis showed that carriers of the rarer G allele had significantly
higher CRP plasma concentrations in CAD(−) subjects (P = 0.031) and higher homocysteine concentrations in CAD(+) group (P < 0.001). Atherosclerosis is an inflammatory disease resulting from different genetic and environmental factors. Results
presented here support the contribution of CRP genetic variations in the development of CAD. 相似文献
12.
Kurnaz O Akadam-Teker AB Yilmaz-Aydoğan H Tekeli A Isbir T 《Molecular biology reports》2012,39(4):4351-4358
In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy
(LVH). The 3′untranslated region (3′UTR) 188CT polymorphism of lectin-like oxidized low-density lipoproteins receptor-1 (LOX-1)
gene has been associated with an increased risk for CAD. We aim to investigate, in a Turkish population, whether 3′UTR188CT
variation could affect the development of LVH in CAD patients. In a population-based case–control study, we compared 83 cases
with CAD and 99 healthy controls for this polymorphism. The LOX-1 3′UTR188CT genotypes were determined by PCR–RFLP technique.
LOX-1 3′UTR188 TT genotype was associated with significantly increased systolic blood pressure (P = 0.047) and risk of LVH (P = 0.014, OR: 3.541) when compared with the C allele carriers. In addition, the TT genotype was positively associated with
decreased levels of HDL-cholesterol in the control subjects (P = 0.031) and increased levels of VLDL-C in the patient group (P = 0.009). The LOX-1 3′UTR188CT gene polymorphism may predispose to the development of LVH in CAD patients, dependent on blood
pressure. 相似文献
13.
14.
Ying-Gang Chen Yan-Long Liu Shi-Xiong Jiang Xi-Shan Wang 《Cell biochemistry and biophysics》2011,59(1):1-6
In current TNM stage system, T4 lesions represent a complex group and should be considered to further optimize the classification.
This study evaluates the significance of adhesion pattern in T4 subclassification based on prognostic analysis of T4N0M0 colorectal
cancer following en bloc multivisceral resection (MVR). Prospectively collected data (1992–2004) were analyzed for 278 patients
with stage T4N0M0 lesions following MVR for colorectal cancer. Patients were divided into inflammatory adhesion (IA) and malignant
invasion (MI) groups based on adhesion to adjacent organs. Survival was evaluated by Kaplan–Meier and Cox proportional hazards
regression analyses. MI was detected in 249 of 460 (54.1%) resected organs and in 159 of 287 (55.40%) patients undergoing
MVR. Compared with IA group, patients in MI group showed no significant difference in clinicopathological data except tumor
differentiation (P = 0.0376). Cox proportional hazards regression showed that MI was independently associated with overall survival among both
colon (HR = 2.028; P = 0.0001) and rectal (HR = 0.451; P = 0.0002) cancer patients. Kaplan–Meier analysis showed that MI patients had a significantly higher MVR compared with IA
patients (colon cancer: P = 0.0018; rectal cancer: P = 0.0116). In conclusion, MI was validated as an adverse prognostic factor for stage T4N0M0 colorectal cancer following MVR
suggesting that it may be classified as a T4-subgroup in order to reinforce practice guidelines. 相似文献
15.
Teresa Warchoł Margarita Lianeri Jan K. Łącki Paweł P. Jagodziński 《Molecular biology reports》2010,37(7):3121-3125
It has been reported that stromal cell-derived factor-1 (SDF1), currently also designated CXCL12, plays a significant role
in the development of nephritis and death in the lupus mice model. Using restriction length fragment polymorphism (RFLP) analysis
we assessed the frequencies of SDF1-3′ G801A (rs 1801157) polymorphic variants between systemic lupus erythematosus (SLE) patients (n = 150) and controls (n = 300). There were no significant differences in the prevalence of SDF1-3′ G801A polymorphic variants in SLE patients and healthy individuals. However, we observed that the SDF1-3′ A/A and G/A genotypes (recessive model) contributed to renal manifestations of SLE OR = 3.042 (95% CI = 1.527–6.058, P = 0.002), and the p value stayed statistically significant after Bonferroni correction (p
corr = 0.032) in SLE patients. We also found an association of the SDF1-3′ A/A and G/A genotypes (recessive model) with dermal manifestations of SLE OR = 2.510 (95% CI = 1.247–5.052, P = 0.0122), (p
corr = 0.1952) but this did not remain statistically significant after Bonferroni correction. Our observations suggest that the
SDF1-3′ G801A genotype may be associated with some clinical manifestations in patients with SLE. 相似文献
16.
Mahir Karakas Jens Baumert Marcus E. Kleber Barbara Thorand Dhayana Dallmeier Günther Silbernagel Tanja B. Grammer Wolfgang Rottbauer Christa Meisinger Thomas Illig Winfried M?rz Wolfgang Koenig 《PloS one》2012,7(12)
Background
Elevated soluble (s) E-selectin levels have been associated with various cardiovascular diseases. Recently, genetic variants in the ABO blood group have been related to E-selectin levels in a small cohort of patients with type 1 diabetes. We evaluated whether this association is reproducible in two large samples of Caucasians.Methodology/ Principal Findings
Data of the present study was drawn from the population-based MONICA/KORA Augsburg study (n = 1,482) and the patients-based LURIC study (n = 1,546). A high-density genotyping array (50K IBC Chip) containing single-nucleotide polymorphisms (SNPs) from E-selectin candidate genes selected on known biology of E-selectin metabolism, mouse genetic studies, and human genetic association studies, was used for genotyping. Linear regression analyses with adjustment for age and sex (and survey in KORA) were applied to assess associations between gene variants and sE-selectin concentrations. A number of 12 SNPs (in KORA) and 13 SNPs (in LURIC), all from the ABO blood group gene, were significantly associated with the log-transformed concentration of E-selectin. The strongest association was observed for rs651007 with a change of log-transformed sE-selectin per one copy of the minor allele of −0.37 ng/ml (p = 1.87×10−103) in KORA and −0.35 ng/ml (p = 5.11×10−84) in LURIC. Inclusion of rs651007 increased the explained sE-selectin variance by 0.256 in KORA and 0.213 in LURIC. All SNPs had minor allele frequencies above 20% showing a substantial gene variation.Conclusions/ Significance
Our findings in two independent samples indicate that the genetic variants at the ABO locus affect sE-selectin levels. Since distinct genome-wide association studies linked the ABO gene with myocardial infarction (MI) in the presence of coronary atherosclerosis and with coronary artery disease, these findings may not only enhance our understanding of adhesion molecule biology, but may also provide a focus for several novel research avenues. 相似文献17.
Ahmed W Malik M Saeed I Khan AA Sadeque A Kaleem U Ahmed N Ajmal M Azam M Qamar R 《Molecular biology reports》2011,38(4):2541-2548
A case–control association study on 229 Myocardial Infarction (MI) patients and 217 healthy controls was carried out to determine
the role of tissue-plasminogen activator (t-PA) (Alu-repeat insertion (I)/deletion (D)) and plasminogen activator inhibitor
(PAI-1) (4G/5G insertion/deletion) polymorphisms with MI in the Pakistani population. In MI patients the genotype distribution
of the PAI-1 gene was not found to be different when compared with the unaffected controls (P > 0.05, χ2 = 1.03). The risk allele 4G was also not associated with MI (P > 0.05, χ2 = 0.46, odds ratio (OR) = 1.1 (95% confidence interval (CI) = 0.84–1.43), P > 0.05). Similarly, the genotype frequencies of t-PA I/I, I/D and D/D were not different from the unaffected controls (P > 0.05, χ2 = 1.60), and the risk allele “I” was not found to be associated with MI (P > 0.05, χ2 = 1.35, OR = 0.86 (95% CI = 0.66–1.11), P > 0.05). However, when the data were distributed along the lines of gender a significant association of the 4G/4G PAI-1 genotype
was observed with only the female MI patients (P < 0.05, z-test = 2.21). When the combined genotypes of both the polymorphisms were analyzed, a significant association of
MI was observed with the homozygous DD/4G4G genotype (P < 0.01, z-test = 2.61), which was specifically because of the female samples (P = 0.01, z-test = 2.53). In addition smoking (P < 0.001, χ2 = 13.52, OR = 3.45 (95% CI = 1.77–6.94)), diabetes (P < 0.001, χ2 = 22.45, OR = 8.89 (95% CI = 2.96–29.95)), hypertension (OR = 7.76 (95% CI = 2.88–22.68), P < 0.001) family history (P < 0.001, χ2 = 13.72, OR = 3.7 (95% CI = 1.71–8.18)) and lower HDL levels (P < 0.05) were found to be significantly associated with the disease. In conclusion the PAI-1 gene polymorphism was found to
have a gender specific role in the female MI patients. 相似文献
18.
M. Parczewski M. Leszczyszyn-Pynka M. Kaczmarczyk G. Adler A. Bińczak-Kuleta B. Łoniewska A. Boroń-Kaczmarska A. Ciechanowicz 《Journal of applied genetics》2009,50(2):159-166
Genetic susceptibility to HIV infection was previously proven to be influenced by some chemokine receptor polymorphisms clustering
on chromosome 3p21. Here the influence of 5 genetic variants was studied: Δ32CCR5, G(-2459)ACCR5, G190ACCR2, G744ACX3CR1 and C838TCX3CR1. They were screened in a cohort of 168 HIV-1 positive adults [HIV(+) group] and 151 newborns [control group] from northwestern
Poland. PCR-RFLP was performed to screen for the variants (except for A32CCR5 polymorphism, where PCR fragment size was sufficient to identify the alleles) and then electrophoresed on agarose gel to
determine fragment size. Distribution of genotypes and alleles was not significantly different between the groups except for
theCCR5 polymorphisms, with the A32 allele and the (-2459)ACCR5 allele more frequent among neonates than in the HIV(+) group. No Δ32/Δ32 homozygotes were found in the HIV(+) group, but
16.1% were Δ32/wt heterozygotes. In the control group, 1.3% were Δ32/Δ32 homozygotes and 26.0% were Δ32/wt heterozygotes.
Linkage between the chemokine polymorphisms was calculated using the most informative loci for haplotype reconstruction. Haplotypes
containing Δ32 CCR5,190GCCR2 and 744ACX3CR1 were found to be significantly more common in the control group. This suggests an association between these haplotypes and
resistance to HIV-1 infection. 相似文献
19.
CX3CR1, an important chemokine receptor in dendritic cells (DCs), is linked to the progression of atherosclerotic plaques.
However, the mechanism(s) determining the role of CX3CR1 in atherosclerosis have not been clearly elucidated. In this study,
we developed DCs from monocytes of Sprague-Dawley (SD) rats in the presence of recombinant human granulocyte–macrophage colony-stimulating
factor (GM-CSF) and recombinant human interleukin-4 (IL-4). The presence of recombinant human TNF-α and LPS forced the cells
to mature. When compared to immature DCs, flow cytometry (FACS) analysis revealed that mature DCs display a sustained increase
in the levels of CD11c, CD86, and CD80 expression. The expression of Fractalkine (FKN) in endothelial cells (ECs) contributes
to the maturation of DCs and expression of CX3CR1. We revealed that mRNA expression levels of CX3CR1 in mature DCs are significantly
higher than those of immature DCs (P < 0.001). Transfection of DCs with siRNA specific for the CX3CR1 gene resulted in potent suppression of gene expression and
inhibition of interactions between DCs and ECs. Based on these data, we hypothesized that CX3CR1 contributes to the DC–EC
interaction. CX3CR1 may serve as a new target molecule for increasing therapeutic interactions in atherosclerosis. 相似文献
20.
Zeynep Ermis Karaali Seyma Sozen Melis Yurdum Canan Cacina Bahar Toptas Ozlem Gok Bedia Agachan 《Molecular biology reports》2010,37(7):3615-3619
Inflammation is a crucial component of coronary atherosclerosis and myocardial infarction (MI). Chemokine receptors are important
modulators of inflammation. Polymorphisms in genes coding for chemokine receptors, CCR2 and CCR5, have been studied as genetic markers of coronary artery
disease. In the present study, we investigated whether genetic variants of CCR2-V64I and CCR5-delta32 chemokine receptors
have any effect on the development of myocardial infarction. A total of 146 MI patients and 202 control subjects were genotyped
for CCR2 and CCR5. CCR2-V64I genotypes were not significantly different between patients with MI and controls (P > 0.05). CCR5-delta32 genotype distribution in cases was significantly different from that of controls (P = 0.042). The CCR5-delta32 wt/deletion genotype frequencies for controls and cases were 0.10 and 0.19, respectively and individuals
with CCR5-delta32 wt/deletion genotype had a 2.13-fold increased risk of myocardial infarction (P = 0.0013). Individuals carrying the CCR5-delta32 heterozygote or homozygous variant genotype (deletion/deletion + wt/deletion)
had a 1.96-fold increased risk of myocardial infarction compared with the wild-type genotype (wt/wt) (p: 0.016). In conclusion,
our data have suggested that genetic variant of CCR5 might be associated with the development of MI. Further larger sample
size studies are required to confirm our findings. 相似文献