Overall and sex-specific associations between methylation of the ABCG1 and APOE genes and ischemic stroke or other atherosclerosis-related traits in a sibling study of Chinese population

Abstract Background Identifying subjects with a high risk of ischemic stroke is fundamental for prevention of the disease. Both genetic and environmental risk factors contribute to ischemic stroke, but the underlying epigenetic mechanisms which mediate genetic and environmental risk effects are not fully understood. The aim of this study was to explore whether DNA methylation loci located in the ATP-binding cassette G1 (ABCG1) and apolipoprotein E (APOE) genes, both involved in the metabolism of lipids in the body, are related to ischemic stroke, using the Fangshan/Family-based Ischemic Stroke Study in China. We also tested if these CpG sites were associated with early signs of cardiovascular atherosclerosis (carotid intima–media thickness (cIMT), ankle–brachial index (ABI), and brachial–ankle pulse wave velocity (baPWV)). Results DNA methylation at the cg02494239 locus in ABCG1 was correlated with ischemic stroke after adjusting for gender, previous history of diabetes and hypertension, smoking, drinking, body mass index, and blood lipid levels (above vs below mean, OR = 2.416, 95% CI 1.024–5.700, P = 0.044; 75–100% percentile vs 0–25% percentile, OR = 4.461, 95% CI 1.226–16.225, P = 0.023). No statistically significant associations were observed for the cg06500161 site in ABCG1 and the cg14123992 site in APOE with ischemic stroke. The study detected that hypermethylation of the ABCG1 gene was significantly associated with cIMT, hypermethylation of the APOE gene was significantly related to ABI, and methylation of the APOE gene was statistically negatively correlated with baPWV. The above relationships demonstrated gender differences. Conclusions These findings suggest that epigenetic modification of ABCG1 and APOE may play a role in the pathway from disturbed blood lipid levels to the development of cardiovascular diseases. Future prospective validation of these findings is warranted.

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PPARG gene C161T CT/TT associated with lower blood lipid levels and ischemic stroke from large-artery atherosclerosis in a Han population in Guangdong

Neurological Research ◽

10.1080/01616412.2016.1189056 ◽

2016 ◽

Vol 38 (7) ◽

pp. 620-624 ◽

Cited By ~ 5

Author(s):

Wei-min Wei ◽

Xiao-yan Wu ◽

Shu-ting Li ◽

QingYu Shen

Keyword(s):

Ischemic Stroke ◽

Blood Lipid ◽

Large Artery ◽

Lipid Levels ◽

Han Population ◽

Lower Blood ◽

Pparg Gene ◽

Blood Lipid Levels

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The Combination of Aerobic and Resistance Exercise Induces Weight Loss via the PGC-1α/Irisin/UCP-1 Pathway

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2019.2123 ◽

2019 ◽

Vol 9 (10) ◽

pp. 1388-1394

Author(s):

Hong Deng ◽

Wei Zhang ◽

Dingguo Ruan ◽

Dezhi Chen ◽

Xiaoyang Xu ◽

...

Keyword(s):

Weight Loss ◽

Body Weight ◽

Resistance Exercise ◽

Aerobic Exercise ◽

Human Subjects ◽

Blood Lipid ◽

The Body ◽

Lipid Levels ◽

Reduced Body ◽

Blood Lipid Levels

Obesity is a modern disease and the cause is quite complicated. This study explores the effects of aerobic and resistance exercise on weight loss and their relationship with the PGC-1α/Irisin/UCP-1 signaling pathway. First, we selected 52 obese students for aerobic and resistance exercise. Second, we established an obesity rat model, and then subjected them to 12 weeks of aerobic and resistance exercise. The body weights and blood lipid contents of all the subjects were measured, and mRNA and protein expressions were determined via real-time PCR and western blot. In obese students, aerobic exercise and the combination of aerobic and resistance exercise significantly reduced body weight and blood lipid levels. In obese model rats, aerobic and resistance exercise significantly reduced the body weight, blood lipid levels, and increased the PGC-1, Irisin, and UCP-1 levels. Furthermore, the combined effects of aerobic and resistance exercise were similar to those of prolonged aerobic exercise in both human subjects and model rats. The mechanism of weight loss via aerobic and resistance exercise may be related to the PGC-1α/Irisin/UCP-1 pathway, and the combination of aerobic and resistance exercise may be a more suitable weight loss option for obese patients.

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A genetic variant in the promoter of lncRNA MALAT1 is related to susceptibility of ischemic stroke

10.21203/rs.2.19452/v1 ◽

2019 ◽

Author(s):

yan wang ◽

Xi-Xi Gu ◽

Hua-Tuo Huang ◽

Chun-Hong Liu ◽

Gui-Jiang Wei ◽

...

Keyword(s):

Ischemic Stroke ◽

Lung Adenocarcinoma ◽

Protective Factor ◽

Genetic Variant ◽

Blood Lipid ◽

Control Group ◽

Lipid Levels ◽

Lncrna Malat1 ◽

Significant Difference ◽

Blood Lipid Levels

Abstract Metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) was aberrantly expressed in diverse diseases including ischemic stroke (IS). This study aimed to investigate the association between MALAT1 polymorphism and IS risk. We performed the genotyping of rs600231, rs1194338, rs4102217 and rs591291 in the promoter of MALAT1 by SNPscan method. Quantitative PCR was used to determine the levels of MALAT1 relative expression. We found the rs1194338 C>A variant in MALAT1 promoter was associated with IS risk (AC vs. CC: adjusted OR = 0.623, 95% CI, 0.417-0.932, P = 0.021; AA vs. CC: adjusted OR = 0.474, 95% CI, 0.226-0.991, P = 0.047; AC/AA vs. CC: adjusted OR = 0.596, 95% CI, 0.406-0.874, P = 0.008; A vs. C adjusted OR = 0.658, 95% CI, 0.487-0.890, P = 0.007). The IS patients showed higher expression levels of MALAT1 compared with the control group ( P < 0.05), but patients with AC/AA genotypes of rs1194338 have no significant difference compared to CC genotype ( P > 0.05). In addition, no significant differences were observed in blood lipid levels among SNPs of MALAT1 ( P > 0.05). These results suggest that the rs1194338 AC/AA genotypes may be a protective factor for IS, which mechanism needs to be further explored.

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