MiR-155 expression was highly elevated in EAM mice. An imbalance of Th17/Treg existed in EAM mice. MiR-155 inhibition in EAM attenuated disease severity and cardiac injury. MiR-155 inhibition suppressed Th17 immune response in EAM. MiR-155 inhibition reduced DC function of secreting Th17-polarizing cytokines in EAM.
Vitamin D receptor (VDR) polymorphisms were indicated to be associated with coronary artery disease (CAD); however, published studies reported inconsistent results.The aim of this meta-analysis is to reach a more accurate estimation of the relationship between VDR genetic polymorphisms and CAD risk.Eligible studies were retrieved by searching PubMed, Embase, VIP, Wanfang and China National Knowledge Infrastructure databases. Included and excluded criteria were formulated. The case group was patients with CAD, and the control group was healthy subjects. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate VDR polymorphisms associations with CAD risk. Heterogeneity was evaluated by Q statistic and I2 statistic.Seven studies of a total of 2306 CAD patients and 4151 control subjects met the inclusion criteria. The pooled results from Taq1 showed increased risk in allelic model (OR = 1.14, 95% CI = 1.02–1.28), dominant model (OR = 1.21, 95% CI = 1.02–1.43), heterozygote model (OR = 1.19, 95% CI = 1.00–1.1.42), and homozygote model (OR = 1.27, 95% CI = 1.01–1.61). Besides, Fok1 T > C showed decreased risk in allelic model (OR = 0.81, 95% CI = 0.65–1.00) and Fok1 A > G also showed decreased risk in allelic model (OR = 0.67, 95% CI = 0.45–1.00) and recessive model (OR = 0.55, 95% CI = 0.31–0.97). In Caucasian subgroup, Bsm1showed increased risk in allelic model (OR = 1.23, 95% CI = 1.02–1.47), heterozygote model (OR = 1.20, 95% CI = 1.00–1.44), and homozygote model (OR = 1.22, 95% CI = 1.02–1.45). In CAD patients with type 2 diabetes mellitus (T2DM), Apa1showed a decreased risk in heterozygote model (OR = 0.80, 95% CI = 0.66–0.98); however, increased risk in recessive model (OR = 5.00, 95% CI = 2.74–9.13) was discovered in CAD patients without T2DM.The Fok1 polymorphism may play a protective role in CAD, and the possible protective role in Apa1 CA genotype in CAD patients with T2DM needs further studies. The Taq1 polymorphism is found to be associated with a significant increase in CAD risk based on our analysis; moreover, increased risk in Apa1 polymorphism in CAD patients without T2DM and Bsm1 polymorphism in Caucasian group is also detected.
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