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Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism Contributes to Ischemic Stroke Risk: A Meta-Analysis of 50 Case-Control Studies  [PDF]
Zhizhong Zhang, Gelin Xu, Dezhi Liu, Xinying Fan, Wusheng Zhu, Xinfeng Liu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0046495
Abstract: Background Many studies have investigated the association between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and risk of ischemic stroke. However, the evidence is inadequate to draw robust conclusions because most studies were generally small and conducted in heterogeneous populations. To shed light on these inconclusive findings, we conducted a large meta-analysis of studies relating the ACE I/D polymorphism to the risk of ischemic stroke. Methods Relevant studies were identified by searching PubMed and Embase through February 2012 and by reviewing the references of retrieved articles. We included studies that reported odds ratio (OR) with 95% confidence interval (CI) for the association between this polymorphism and ischemic stroke risk. Results Fifty independent publications, with 10 070 stroke cases and 22 103 controls, were included. The results indicated that the DD homozygote carriers had a 37% higher risk of ischemic stroke when compared with the homozygotes II and heterozygote ID [odds ratio (OR) = 1.37, 95% confidence interval (CI): 1.22–1.53]. Subgroup analyses indicated that this higher risk was more pronounced among Asians, hospital-based studies, and small vessel disease (SVD). Potential publication bias may exist, but correction for this bias using a formal statistical method did not materially alter the combined risk estimate. Conclusion The results of our meta-analysis indicate that the D allele of ACE I/D polymorphism is a low-penetrance susceptibility marker of ischemic stroke.
Lack of an Association between CYP11B2 C-344T Gene Polymorphism and Ischemic Stroke: A Meta-Analysis of 7,710 Subjects  [PDF]
Yan Pi, Li-li Zhang, Kai Chang, Lu Guo, Yun Liu, Bing-hu Li, Xiao-jie Cao, Shao-qiong Liao, Chang-yue Gao, Jing-cheng Li
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068842
Abstract: Background The association between aldosterone synthase (CYP11B2) C-344T gene polymorphism and ischemic stroke remains controversial and ambiguous. To better explain the association between CYP11B2 polymorphism and ischemic stroke risk, a meta-analysis was performed. Methods Based on comprehensive searches of Medline, Embase, Web of Science, CNKI and CBM databases, we identified and abstracted outcome data from all articles to evaluate the association between CYP11B2 polymorphism and ischemic stroke. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were performed in all genetic models. Fixed or random effects model was separately used depending on the heterogeneity between studies. Publication bias was tested by Begg's funnel plot and Egger's regression test. Results A total of 12 studies including 3,620 ischemic stroke cases and 4,090 controls were identified. There was no statistical evidence of association between CYP11B2 C-344T polymorphism and ischemic stroke in all genetic models (allelic model: OR = 1.19, 95% CI = 0.95–1.49; additive model: OR = 1.43, 95% CI = 0.91–2.27; dominant model: OR = 1.30, 95% CI = 0.89–1.89; and recessive model: OR = 1.24, 95% CI = 0.96–1.60). On subgroup analysis by ethnicity, similarly results were found in both Asians and non-Asians. For Asians, the combined ORs and 95% CIs were (allelic model: OR = 1.07, 95% CI = 0.87–1.32; additive model: OR = 1.15, 95% CI = 0.77–1.71; dominant model: OR = 1.13, 95% CI = 0.92–1.38; and recessive model: OR = 1.09, 95% CI = 0.84–1.40). For none-Asians, the combined ORs and 95% CIs were (allelic model: OR = 1.58, 95% CI = 0.90–2.76; additive model: OR = 2.37, 95% CI = 0.79–7.05; dominant model: OR = 1.79, 95% CI = 0.77–4.19; and recessive model: OR = 1.80, 95% CI = 0.96–3.36). Conclusion The present meta-analysis suggested that CYP11B2 C-344T polymorphism was unlikely contribute to ischemic stroke susceptibility.
Association between Transforming Growth Factor-Beta 1 T869C Polymorphism and Ischemic Stroke: A Meta-Analysis  [PDF]
Lingmei Peng, Peng Li, Jian Chen, Ke Yan, Fuyuan Huo, Lina Han, Can Li, Sheng Tan, Xiaodan Jiang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067738
Abstract: Objective To explore the association between transforming growth factor-beta1 (TGF-β1) T869C polymorphism and risk of ischemic stroke (IS) by performing a meta-analysis based on published articles. Methods Systematic electronic searches of PubMed, Science Direct, BIOSIS Previews, Chinese Biomedical Database, Chinese National Knowledge Infrastructure, and WANFANG Database were performed. The strength of the association was calculated by pooled odds ratios (ORs) with 95% confidence intervals (95%CIs). Subgroup analysis was conducted to explore potential sources of heterogeneity. Sensitivity analysis was performed to elucidate the stability of the outcomes. Publication bias was evaluated by Begg’s funnel plot and Egger’s test. Results A total of 6 studies involving 1701 cases were included. The overall estimates did not show any significant association between TGF-β1 T869C polymorphism and risk of IS under all genetic models (C vs. T: OR = 1.08,95%CI = 0.88–1.32; CC vs. TT:OR = 1.17,95%CI = 0.79–1.72; CT vs. TT: OR = 0.91, 95%CI = 0.68–1.22; CC+CT vs. TT: OR = 0.99, 95%CI = 0.73–1.35; CC vs. CT+TT: OR = 1.23, 95%CI = 0.95–1.59). Similar lacking associations were observed in subgroup analysis based on ethnicity and source of controls. When stratified by study design, significant increased association of IS risk was found in cohort studies under genetic models except recessive model(C vs. T: OR = 1.18, 95%CI = 1.05–1.32; CC vs. TT: OR = 1.40, 95%CI = 1.10–1.77; CT vs. TT: OR = 1.23, 95%CI = 1.02–1.49; CC+CT vs. TT: OR = 1.27, 95%CI = 1.03–1.57; CC vs. CT+TT, OR = 1.21, 95%CI = 0.99–1.47), whereas in case-control studies a significant decreased risk was detected under heterozygote comparison(CT vs. CC: OR = 0.72, 95%CI = 0.57–0.92). However, after correction for multiple testing, the associations were observed to be null significant in both cohort and case-control subgroups among all genetic models. Conclusion This meta-analysis suggested that current epidemiological studies of TGF-β1 T869C polymorphism are too inconsistent to draw a conclusion on the association with IS susceptibility. Given the small sample size and remarkable between-study heterogeneity, further well-designed prospective large-scale studies are warranted.
Relationship between Interleukin-10 ?1082A/G Polymorphism and Risk of Ischemic Stroke: A Meta-Analysis  [PDF]
Jun Jin, Wuying Li, Lingmei Peng, Jian Chen, Rong Li, Peihua Wu, Sheng Tan
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094631
Abstract: Objective To analyze the association between ?1082A/G polymorphism in interleukin-10 (IL-10) gene and ischemic stroke (IS) risk by meta-analysis. Methods We carried out a systematic electronic search in PubMed, BIOSIS Previews, Science Direct, Chinese National Knowledge Infrastructure, Chinese Biomedical Database, Weipu database and WANGFANG Database. Pooled odds ratios (ORs) with 95% confidence intervals (95%CIs) were calculated to assess the strength of the association. Results 7 studies were included. There was no significant association between IL-10 ?1082A/G polymorphism and IS risk under all genetic models in overall estimates (A vs. G: OR = 1.23,95%CI = 0.85–1.79;AA vs. GG: OR = 1.01,95%CI = 0.47–2.19; AG vs. GG: OR = 0.76, 95%CI = 0.38–1.55; AA+AG vs. GG: OR = 0.89,95%CI = 0.46–1.73; AA vs. AG+GG: OR = 1.39, 95%CI = 0.91–2.13). Similarly, no associations were found in subgroup analysis based on ethnicity and source of controls. However, removing the study deviating from Hardy–Weinberg equilibrium (HWE) produced statistically significant associations for overall estimates under recessive model(AA VS. AG+GG OR 1.58, 95% CI 1.04–2.42) and among Asians in all genetic models (A VS.G OR 1.64, 95% CI 1.07–2.53; AA vs. GG OR1.91, 95% CI 1.31–2.80; AG vs. GG OR1.44, 95% CI 1.09–1.91; AA+AG vs. GG OR 1.54, 95% CI 1.18–2.01;AA VS. AG+GG OR 1.79, 95% CI 1.07–3.00). Even after Bonferroni correction, the associations were observed still significantly in Asians under the two models (AA vs. GG OR1.91, 95% CI 1.31–2.80, P = 0.0008; AA+AG vs. GG OR 1.54, 95% CI 1.18–2.01, P = 0.001). Conclusion This meta-analysis indicates that IL10 ?1082 A/G polymorphism is associated with IS susceptibility in Asians and the ?1082 A allele may increase risk of IS in Asians. Considering the sample size is small and between-study heterogeneity is remarkable, more studies with subtle design are warranted in future.
Peroxisome proliferator-activated receptor gamma-2 P12A polymorphism and risk of acute myocardial infarction, coronary heart disease and ischemic stroke: A case-cohort study and meta-analyses  [cached]
Mohammad Hadi Zafarmand,Yvonne T van der Schouw,Diederick E Grobbee,Peter W de Leeuw
Vascular Health and Risk Management , 2008,
Abstract: Mohammad Hadi Zafarmand1,3, Yvonne T van der Schouw1, Diederick E Grobbee1, Peter W de Leeuw2, Michiel L Bots11Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Heidelberglaan 100, Str 6.131, 3584 CX, Utrecht, The Netherlands; 2Department of Internal Medicine, University Hospital Maastricht, PO Box 5800, NL-6202 AZ, Maastricht, The Netherlands; 3Persian Gulf Health Research Center, Department of Genomic Health, Bushehr University of Medical Sciences and Health Services, Moalem Street, Po Box 3631, Bushehr, IranBackground: The alanine allele of P12A polymorphism in PPARG gene in a few studies has been associated with a reduced or increased risk of acute myocardial infarction (AMI). Yet, the risk relation has not been confirmed, and data on ischemic stroke (IS) is scarce. We therefore investigated the role of this polymorphism on occurrence of AMI, coronary heart disease (CHD) and IS.Methods and findings: We performed a case-cohort study in 15,236 initially healthy Dutch women and applied a Cox proportional hazards model to study the relation of the P12A polymorphism and AMI (n = 71), CHD (n = 211), and IS (n = 49) under different inheritance models. In addition, meta-analyses of published studies were performed. Under the dominant inheritance model, carriers of the alanine allele compared with those with the more common genotype were not at increased or decreased risk of CHD (hazard ratio [HR] = 0.82; 95% confidence interval [CI], 0.58 to 1.17) and of IS (HR = 1.03; 95% CI, 0.14 to 7.74). In addition no relations were found under the recessive and additive models. Our meta-analyses corroborated these findings by showing no significant association. For AMI we found a borderline significant association under dominant (HR = 0.49; 95% CI, 0.26 to 0.94), and additive (HR = 0.51; 95% CI, 0.26 to 1.00) models which could be due to chance, because of small cases in this subgroup. The meta-analysis did not show any association between the polymorphism and risk of AMI under the different genetic models.Conclusions: Our study in healthy Dutch women in combination with the meta-analyses of previous reports does not provide support for a role of P12A polymorphism in PPARG gene in MI and CHD risk. Also our study shows that the polymorphism has no association with IS risk.Keywords: genetics, myocardial infarction, polymorphism, PPARG gene, risk factors, population-based
Lentiviral-Mediated shRNA Silencing of PDE4D Gene Inhibits Platelet-Derived Growth Factor-Induced Proliferation and Migration of Rat Aortic Smooth Muscle Cells  [PDF]
Lin Liu,Xiaowei Xu,Jiejie Li,Xia Li,Wenli Sheng
Stroke Research and Treatment , 2011, DOI: 10.4061/2011/534257
Abstract: Phosphodiesterase 4D (PDE4D) is a member of the large superfamily of phosphodiesterases. PDE4D polymorphisms have been found to associate with ischemic stroke. Proliferation and migration of vascular smooth muscle cells (VSMCs) play a critical role in the pathogenesis of atherosclerosis. In this study, infection of VSMCs with lentivrius particles carrying shRNA direct against PDE4D significantly inhibited platelet-derived growth factor-induced VSMC proliferation and migration, and the inhibitory effects were not associated with global intracellular cAMP level. Our results implicate that PDE4D has an important role in VSMC proliferation and migration which may explain its genetic susceptibility to ischemic stroke. 1. Introduction Stroke, a complex disease, remains the third common cause of death behind heart disease and cancer and is the leading cause of disability in developed countries as well as in China. Ischemic stroke accounts for up to 80% of all strokes. Both environmental factors and genetic variants contribute to stroke. Although several genetic defects have been identified in rare forms of stroke, the genetic causes of common forms of ischemic stroke remain elusive. Recently, PDE4D has been identified as the first gene linked to common forms of stroke [1]. However, subsequent studies have produced inconsistent results for the association [2–9]. Due to the variable results, several meta-analyses on the gene have been accomplished, which also drew conflicting conclusions [10–13]. Racial differences might be responsible for the inconsistent results. Therefore, experimental studies on function of PDE4D will help to unveil the puzzle. PDE4D belongs to a large superfamily of PDEs which are the only hydrolytic enzymes of cAMP and key signal transduction molecules in multiple cell types, including vascular smooth muscle cells. Eleven families (PDE1–PDE11) have been identified in the large superfamily of PDEs [14]. There are four major families found in VSMCs: PDE1, PDE5, PDE3, and PDE4. PDE1 and PDE5 are mainly responsible for cGMP-hydrolyzing activity, whereas PDE3 and PDE4 contribute to most of cAMP-hydrolyzing activity [15, 16]. PDE4 has four subfamilies: PDE4A, 4B, 4C, and 4D, which are differentially localized between cells [17]. PDE4D is expressed broadly in many kinds of cell [18, 19]. In arterial VSMCs, PDE4D is dominantly expressed and degrades second-messenger cAMP[20]. Recent studies suggest that PDE4D may have a critical role in atherosclerosis. For example, PDE4D is largely associated with atherosclerotic stroke such as cardiogenic and
Role of MTHFR C677T polymorphism in ischemic stroke  [cached]
Panigrahi Inusha,Chatterjee Tathagata,Biswas Arijit,Behari Madhuri
Neurology India , 2006,
Abstract: Background: Homozygosity for MTHFR C677T polymorphism can lead to significantly high homocysteine levels and hyperhomocysteinemia is an important risk factor for thrombotic events. Aims: The aim was to determine role of MTHFR C677T polymorphism in North Indians with ischemic stroke. Settings and Design: In a prospective study, the subjects of stroke were recruited from the neurology clinic of the hospital. Controls were healthy individuals from the Hematology clinic without any history of stroke. Materials and Methods: Plasma homocysteine levels were measured by enzyme immuno assay method after 3 months of acute episode. Serum folate and Vitamin B12 levels were estimated by competitive inhibition radioassay. MTHFR polymorphism was detected by PCR-RFLP using Hinf I enzyme. Statistical analysis: The analysis of significance of results was done using SPSS software package. A pvalue < 0.05 was taken as significant. Results: Thirty-two acute ischemic stroke patients (aged 1-44 years) were studied. Fourteen (43.8%) had recurrent stroke. Nine (28%) had multiple infarcts. Four of 32 patients (12.5%) had high homocysteine levels. Three out of these 4 hyper-homocysteinemia patients were homozygous ( TT ) for MTHFR polymorphism (2 with recurrent stroke). Two of three homozygous cases with TT genotype had low serum folate. Five of 32 stroke cases (18.8%) were heterozygous ( CT ) genotype. Conclusions: Primary hyper-homocysteinemia appears to be an important risk factor for ischemic stroke in North Indians, most due to MTHFR C677T homozygosity. Folate levels may modify the presentation of the MTHFR TT genotype.
Endothelial NO Synthase Gene Polymorphisms and Risk of Ischemic Stroke in Asian Population: A Meta-Analysis  [PDF]
Meiyun Wang, Xiubo Jiang, Wenlong Wu, Dongfeng Zhang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060472
Abstract: Background The association between polymorphism 4b/a, T-786C and G894T in endothelial NO synthase gene (eNOS) and ischemic stroke (IS) remains controversial in Asian. A meta-analysis was performed to better clarify the association between eNOS gene and IS risk. Methods Based on the search of PubMed, Web of Science (ISI), CNKI (National Knowledge Infrastructure), Wan Fang Med Online and CBM (Chinese Biology Medical Literature Database) databases, all eligible case-control or cohort studies were identified. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) from fixed and random effect models were calculated. Heterogeneity among studies was evaluated using the I2. Meta-regression was used to explore the potential sources of between-study heterogeneity. Begg's test was used to estimate publication bias. Results Our study included 27 articles, contained 28 independent case–control studies, involved a total of 3,742 cases and 3,691 controls about 4b/a, 1,800 cases and 1,751 controls about T-786C and 2,747 cases and 2,872 controls about G894T. A significant association of 4a allele with increased risk of IS was found in dominant (FEM: OR = 1.498, 95% CI = 1.329–1.689), recessive (FEM: OR = 2.132, 95% CI = 1.383–3.286) and codominant (REM: OR = 1.456, 95% CI = 1.235–1.716) models. For T-786C and G894T, there were significant associations with dominant and codominant genetic models, but not with recessive genetic model. Conclusions The meta-analysis indicated that eNOS gene 4b/a, T-786C, G894T polymorphism might be associated with IS.
Low Ankle Brachial Index in Acute Ischemic Stroke: Does ApoE Gene Polymorphism Have a Role?  [PDF]
Shaimaa El-Jaafary, Mohamed El-Tamawy, Hassan Hosny, Mona Fathy, Foad Abd-Allah, Ehab Shaker
World Journal of Cardiovascular Diseases (WJCD) , 2015, DOI: 10.4236/wjcd.2015.52006
Abstract: Background: The existence of asymptomatic peripheral arterial disease among patients with acute ischemic stroke has been studied and proved. Low ankle brachial index (ABI) is considered as a marker of atherosclerosis, and its relation to stroke severity was documented in some studies. The effect of different alleles of ApoE gene on acute ischemic stroke presentation in patients with low ABI is not known. Objective: To study the effect of ApoE gene polymorphism on stroke severity, outcome and recurrence in patients with asymptomatic peripheral arterial disease identified by low ABI. Methods: Patients with acute ischemic stroke were screened for the presence of asymp-tomatic peripheral arterial disease by estimating the ABI using a pocket Doppler ultrasound device. Assay of ApoE gene was done using the real-time PCR technique. Results: Low ABI was present in 31% of patients with acute ischemic stroke. There was no significant difference among patients with different ApoE alleles regarding the severity of their symptoms. Also, there was no significant difference among patients with normal ABI and those with abnormal ABI regarding the ApoE gene polymorphism. Conclusion: The current study showed that there was no significant relation between ApoE gene polymorphism and low ABI in ischemic stroke patients who had asymptomatic peripheral arterial disease.
Association between NADPH Oxidase p22phox C242T Polymorphism and Ischemic Cerebrovascular Disease: A Meta-Analysis  [PDF]
Bing-Hu Li, Li-Li Zhang, Bei-Bei Zhang, Yan-Wei Yin, Li-Meng Dai, Yan Pi, Lu Guo, Chang-Yue Gao, Chuan-Qin Fang, Jing-Zhou Wang, Jing-Cheng Li
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056478
Abstract: Background Epidemiological studies have evaluated the association between nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p22phox C242T polymorphism and risk of ischemic cerebrovascular disease (ICVD), but the results remain inconclusive. This meta-analysis was therefore designed to clarify these controversies. Methodology/Principal Findings Systematic searches of electronic databases Embase, PubMed and Web of Science, as well as hand searching of the references of identified articles and the meeting abstracts were performed. Statistical analyses were performed using software Review Manager (Version 5.1.7) and Stata (Version 11.0). The pooled odds ratios (ORs) with 95% confidence intervals (95%CIs) were performed. Fixed or random effects model was separately used depending on the heterogeneity between studies. Publication bias was tested by Begg's funnel plot and Egger's regression test. A total of 6 studies including 1,948 cases and 2,357 controls were combined showing no statistical evidence of association between NADPH oxidase p22phox C242T polymorphism and overall ICVD (allelic model: OR = 1.08, 95%CI = 0.93–1.26; additive model: OR = 1.33, 95%CI = 0.81–2.17; dominant model: OR = 1.00, 95%CI = 0.86–1.15; recessive model: OR = 1.06, 95%CI = 0.77–1.45). Significant association was found in large-artery atherosclerotic stroke subgroup (allelic model: OR = 1.12, 95%CI = 0.88–1.41; additive model: OR = 1.36, 95%CI = 0.60–3.09; dominant model: OR = 1.25, 95%CI = 0.74–2.11; recessive model: OR = 2.17, 95%CI = 1.11–4.23). No statistical evidence of significant association was observed for small-vessel occlusive stroke, as well as Asian subgroup and Caucasian subgroup. Statistical powers on the combined sample size (total and subgroup) were all lower than 80%. Conclusions/Significance This meta-analysis indicates that NADPH oxidase p22phox C242T polymorphism is more associated with large-artery atherosclerotic stroke than small-vessel occlusive stroke. However, this conclusion should be interpreted with caution due to the small sample size. Larger sample-size studies with homogeneous ICVD patients and well-matched controls are required.
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