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Abstract.In some GWAs studies, GALNT2 and APOE polymorphisms have been identified to be related to alterations of plasma or serum HDL-C and TG concentrations. The purpose of our study is to assess the contribution of GALNT2 rs4846914, APOE rs429358, rs7412, rs405509 variants, and several environmental factors to the development of hypertension disease in the China Han population. A hospital-based case-control study was conducted. Cases were hypertension (n=211) and controls were normal participants (n=434). The AA, AG, and GG genotype frequencies of GALNT2 rs4846914 were 22.8%, 43.1%, and 34.1% in hypertension subjects, and 35.3%, 44.2%, and 20.5% in controls (P<0.05), respectively. The OR of the AG genotype adjusted for all risk factors compared to the AA genotype was 1.61 (95%CI: 1.02 to 2.56) and to the GG genotype 2.67 (95%CI: 1.59 to 4.488). There was no significant difference between the APOE rs429358, rs7412, and rs405509 genotype frequencies in hypertension and control subjects. The present work indicates that SNP rs4846914 in GALNT2 gene is related to an increased risk of hypertension in China Han population, but the APOE gene is not.

Objectives: This study aimed to investigate the relationship between the presence of carotid arteriosclerosis (CAS) and blood pressure variability (BPV) in patients with essential hypertension. Methods:One hundred and forty four essential hypertension patients underwent ambulatory BP monitoring for 24 hours after hospitalization. Common BPV metrics were calculated. General clinical parameters, including age, gender, height, weight, history of coronary heart disease, stroke, diabetes, hypertension, smoking and drink, were recorded. Biochemical indices were obtained from a blood test. Carotid intima-media thickness (IMT) and carotid plaques were assessed to separate patients into a non-CAS group (IMT0.9 mm; n=82) and a CAS group (IMT>0.9 mm; n=62). BPV metrics and clinical parameters were analyzed and compared between the two groups.

BackgroundTransforming growth factor (TGF)-β1 is involved in the pathogenesis of coronary artery disease (CAD), but the mechanism of its action remains unclear. Our study aimed to investigate the role of TGF-β1 in CAD and to explore the possible mechanisms.Material/MethodsA total of 60 CAD patients and 54 healthy people were included in this study. Blood samples were drawn from each participant to prepare serum. ELISA was utilized to measure serum level of TGF-β1. TGF-β1 expression vector, TGF-β1 siRNA, and TIMP-1 siRNA were transfected into human primary coronary artery endothelial cell (HCAEC) line cells, and expression of TGF-β1 sphingosine kinase 1 (SPHK1) and TIMP metallopeptidase inhibitor 1 (TIMP-1) was detected by Western blot. Cell apoptosis was detected by MTT assay.ResultsSerum level of TGF-β1 was specifically higher in patients with CAD than in healthy controls. Serum levels of active TGF-β1 can be used to effectively distinguish CAD patients from healthy controls. TGF-β1 overexpression promoted the apoptosis of HCAEC and TGF-β1 siRNA silencing inhibited the apoptosis of HCAEC. TGF-β1 overexpression also promoted the expression of SPHK1 and TIMP-1. SPHK1 overexpression upregulated TIMP-1 but it showed no significant effects on TGF-β1. TIMP-1 overexpression showed no significant effects on TGF-β1 or SPHK1. SPHK1 inhibitor and TIMP-1 silencing reduced the enhancing effects of TGF-β1 overexpression on cell apoptosis.ConclusionsTGF-β1 appears to promote CAD through the induction of cell apoptosis by upregulating SPHK1 expression and further upregulating its downstream TIMP-1.

Myocardial ischemia‑reperfusion (I/R) injury is a major cause of cardiovascular disease worldwide, and microRNAs have been implicated in the regulation of pathological and physiological processes in myocardial I/R injury. The present study aimed to investigate the role of microRNA (miR)‑221‑3p in myocardial I/R injury. Cell death and lactate dehydrogenase (LDH) activity were increased in hydrogen peroxide (H2O2)‑treated H9c2 cells, as measured by flow cytometry and an LDH detection kit. The expression of miR‑221‑3p was elevated in H2O2‑incubated cells and in remote areas of the rat I/R model, examined using reverse transcription‑quantitative polymerase chain reaction analysis. The overexpression of miR‑221‑3p enhanced the number of propidium iodide (PI)+ cells and the activity of LDH in H2O2‑treated cells. In I/R‑induced rats, the overexpression of miR‑221‑3p promoted the number of myosin+ cells and inhibited the fractional shortening of left ventricular diameter (FSLVD%). The results showed that the expression of p57 at the gene and protein levels was decreased in H9c2 cells incubated with H2O2 and in rats subjected to I/R surgery; the expression of p57 decreased following the overexpression of miR‑221‑3p. Subsequently, the hypothesis that p57 was the direct target of miR‑221‑3p was confirmed by performing a dual‑luciferase reporter assay. Finally, to examine the function of p57 in myocardial impairment, p57 was transfected into H9c2 cells and administered to the rats prior to undergoing H2O2 treatment and I/R surgery, respectively. The results indicated that p57 attenuated the number of PI+ cells and the activity of LDH in H2O2‑treated cells, whereas p57 downregulated the number of myosin+ cells and upregulated FSLVD% in the I/R‑treated rats. Therefore, these findings suggested that miR‑221‑3p exacerbated the H2O2‑induced myocardial damage in H9c2 cells and myocardial I/R injury in the rat model by modulating p57.