Urotensin II activates the ferroptosis pathway through circ0004372/miR-124/SERTAD4 to promote the activation of vascular adventitial fibroblasts.

Both vascular adventitial fibroblasts (VAFs) and urotensin II (UII) play important roles in vascular remodeling diseases, but the mechanism of UII in VAFs is still unclear. UII inhibited miR-124 expression through up-regulating circ0004372 expression, thereby promoting SERTAD4 expression. UII significantly promoted the generation of ROS, MDA and 4-HNE, reduced the activities of SOD, GST and GR, increased Fe2+ concentration and inhibited GPX4 expression through circ0004372/miR-124/SERTAD4.

Glutamine switches vascular smooth muscle cells to synthetic phenotype through inhibiting miR-143 expression and upregulating THY1 expression.

Aims: Vascular smooth muscle cells (VSMCs) are involved in the pathogenesis of many human cardiovascular diseases. They modulate their phenotype from "contractile" to "synthetic" in response to changes in local environmental cues. How glutamine regulates the differentiation of VSMCs and the underlying mechanisms remain largely unknown.

Tanshinone IIA attenuates high glucose induced human VSMC proliferation and migration through miR-21-5p-mediated tropomyosin 1 downregulation.

The proliferation and migration of vascular smooth muscle cells (VSMCs) play important roles in the development and progression of diabetes-related vascular complications. Recently, microRNAs (miRNAs) have been suggested to be involved in the pathogenesis of vascular diseases. This study was designed to investigate the influences of tanshinone IIA, an active compound extracted from Chinese herb Salvia miltiorrhiza, on the proliferation and migration of human aortic VSMCs (HASMCs).

LncRNA-MIAT regulates fibrosis in hypertrophic cardiomyopathy (HCM) by mediating the expression of miR-29a-3p.

Aim: This study aimed to investigate the molecular mechanism underlying the fibrosis in hypertrophic cardiomyopathy (HCM).

Method: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure the expression of potentially relevant microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) in patients with HCM suffering from fibrosis and patients with HCM free of fibrosis. In addition, the regulatory relationship between lncRNAs and miR-29a was studied using a luciferase assay.

Circ-SATB2 upregulates STIM1 expression and regulates vascular smooth muscle cell proliferation and differentiation through miR-939.

The prevention and treatment of coronary heart disease (CHD) is a difficult problem to be solved. More and more studies have found that circular RNAs (circRNAs) may play important roles in the development of CHD. Here detection of vascular smooth muscle cells (VSMCs) showed that circ-SATB2 and STIM1 were up-regulated in proliferative VSMCs, while miR-939 were down-regulated.

[Geographical distribution of the Serum creatinine reference values of healthy adults].

Objective: To explore the relationship between serum creatinine (Scr) reference values in healthy adults and geographic factors and provide evidence for establishing Scr reference values in different regions.

Methods: We collected 29 697 Scr reference values from healthy adults measured by 347 medical facilities from 23 provinces, 4 municipalities and 5 autonomous regions. We chose 23 geographical factors and analyzed their correlation with Scr reference values to identify the factors correlated significantly with Scr reference values.

Effects of monocyte-endothelium interactions on the expression of type IV collagenases in monocytes.

The adhesion of monocytes to endothelial cells is one of the early stages in the development of atherosclerosis. The expression of type IV collagenases, which include matrix metalloproteinase (MMP)-2 and MMP-9, in monocytes is hypothesized to play an important role in monocyte infiltration and transformation into foam cells. The aim of the present study was to examine the effects of monocyte-endothelium interactions on the expression levels of type IV collagenases and their specific inhibitors in monocytes, and to investigate the roles of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in this process.

PI3K/AKT signaling pathway plays a role in enhancement of eNOS activity by recombinant human angiotensin converting enzyme 2 in human umbilical vein endothelial cells.

The aim of this study was to investigate the effect of PI3K/AKT signaling pathway in the activity of recombinant human angiotensin converting enzyme 2 (rhACE2) promoted the activity of endothelial nitric oxide synthase (eNOS). The human umbilical vein endothelial cells (HUVEC) were cultured in vitro. Then treated with Ang II (1×10(-6) mol/L) for 24 h.

Effect of peroxisome proliferator activated receptor γ agonist on angiotensin converting enzyme 2 mRNA expression in monocyte-derived macrophages of essential hypertensive patients.

Objective: To study the effect of peroxisome proliferator activated receptor γ (PPAR-γ) agonist on the angiotensin converting enzyme 2 (ACE2) mRNA expression in monocyte-derived macrophages of essential hypertensive patients.

Methods: Totally 57 essential hypertensive patients were randomly divided into three groups: conventional treatment group (n=18), telmisartan group (n=19), and benazepril group (n=20); 20 patients with normal blood pressure were also selected as the control group. Monocyte-derived macrophages were isolated from blood samples of patients in all four groups.

[Comparison between anti-ouabain egg yolk(IgY) and rabbit antibody(IgG) in enzyme-linked immunosorbent assay].

Aim: To improve specificity and accuracy of endogenous ouabain measurement assay.

Methods: Anti-ouabain polyclonal antibody egg yolk (IgY) and anti-ouabain rabbit antibody (IgG) were prepared respectively. In the presence of two kinds of antibody, then the specificity and accuracy of enzyme-linked immunosorbent assay (ELISA) were compared.

[Peroxisome proliferator-activated receptor activator troglitazone inhibits angiotensin II-stimulated secretion of vasoactive factors by endothelial cells].

Objective: To investigate the effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligand on angiotensin II (AngII)-induced endothelin-1 (ET-1) and NO secretion by endothelial cells in comparison with AngII type I receptor (AT1R) antagonist losartan, so as to reveal the relationship between PPAR gamma and essential hypertension.

Methods: Cultured human umbilical vein endothelial cells (HUVECs) were treated with AngII, PPAR gamma ligand troglitazone, AngII plus troglitazone, and AngII plus AT1R antagonist losartan, respectively, and the concentrations of NO and ET-1 in the cell culture supernatant were measured to evaluate the effects of troglitazone and losartan on AngII-induced NO and ET-1 production by human endothelial cells.

Results: Treatment of the HUVECs with troglitazone at 10 micromol/L and 50 micromol/L did not produce significant changes in ET-1 concentration in the cell culture supernatants, but significantly increased NO concentration as compared with the control group (P<0.