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Long non-coding RNA HOXA11-AS participated in heart disease. In this study, we aim to evaluate the potential roles of HOXA11-AS in atherosclerosis and its underlying mechanisms.The expression levels of HOXA11-AS in ox-LDL-treated HUVECs and arch tissues of high-fat diet-fed ApoEHOXA11-AS contributed to atherosclerotic injuries by directly regulating the miR-515-5p/ROCK1 axis. This study provided new evidence that HOXA11-AS might be a candidate for atherosclerosis therapy.

To observe the relationship between abdominal obesity and left ventricular weight/function.A total of 495 patients [265 males, mean age (55 +/- 12) years] with hypertension (139), diabetes (65), metabolic syndrome (285), diabetes complicated with hypertension (11) were enrolled in this study. Visceral adipose area (VA), the subcutaneous adipose (SA), the total abdominal adipose (TA) were measured by computerized tomography (CT) and left ventricular weight and function were obtained by echocardiography. Patients were divided into three groups according to the VA (I. VA75 cm(2), n=173, II. VA75 and110 cm(2), n=153, III. VAor= 110 cm(2), n=169).Left ventricular mass (LVM) and LVM index (LVMI) increased and LVEF and E/A decreased in proportion to increasing VA. Left ventricular hypertrophy (LVH) rate was significantly higher in group II and III compared to group I and LVEF was significantly reduced in group III compared to group I and II. There are significant correlation between LVMI and VA, SA, TA as well as between LVEF and VA after adjusting gender, age and blood pressure. Logistic regression analysis showed that VA is an independent predictor for LVH.The abdominal adipose accumulation is closely related to the left ventricular weight and function.

We tested the hypothesis that activation of transient receptor potential vanilloid type-1 (TRPV1) by capsaicin prevents adipogenesis. TRPV1 channels in 3T3-L1-preadipocytes and visceral adipose tissue from mice and humans were detected by immunoblotting and quantitative real-time RT-PCR. The effect of TRPV1 on cytosolic calcium was determined fluorometrically in 3T3-L1-preadipocytes and in human visceral fat tissue. Adipogenesis in stimulated 3T3-L1-preadipocytes was determined by oil red O-staining of intracellular lipid droplets, triglyceride levels, expression of peroxisome proliferator-activated receptor-γ, and expression of fatty acid synthase. Long-term feeding experiments were undertaken in wild-type mice and TRPV1 knockout mice. We detected TRPV1 channels in 3T3-L1-preadipocytes and visceral adipose tissue from mice and humans. In vitro, the TRPV1 agonist capsaicin dose-dependently induced calcium influx and prevented the adipogenesis in stimulated 3T3-L1-preadipocytes. RNA interference knockdown of TRPV1 in 3T3-L1-preadipocytes attenuated capsaicin-induced calcium influx, and adipogenesis in stimulated 3T3-L1-preadipocytes was no longer prevented. During regular adipogenesis TRPV1 channels were downregulated which was accompanied by a significant and time-dependent reduction of calcium influx. Compared with lean counterparts in visceral adipose tissue from obese db/db and ob/ob mice, and from obese human male subjects we observed a reduced TRVP1 expression. The reduced TRPV1 expression in visceral adipose tissue from obese humans was accompanied by reduced capsaicin-induced calcium influx. The oral administration of capsaicin for 120 days prevented obesity in male wild type mice but not in TRPV1 knockout mice assigned to high fat diet. We conclude that the activation of TRPV1 channels by capsaicin prevented adipogenesis and obesity.