MiR-3646 accelerates inflammatory response of Ang II-induced hVSMCs via CYP2J2/EETs axis in hypertension model.

Background: Inflammatory response of human vascular smooth muscle cells (hVSMCs) is a driving factor in hypertension progression. It has been reported that miR-3646 was significantly up-regulated in serum samples from patients with coronary artery disease and acute myocardial infarction mice. However, its role and underlying molecular mechanism related to inflammatory response of angiotensin II (Ang II)-induced hVSMCs remain unclear.

Personalized antihypertensive treatment guided by pharmacogenomics in China.

Background: The implementation of genotyping for anti-hypertensive drugs in clinical practice remains a challenge. We conducted this study to analyze the distribution of polymorphisms of antihypertensive drug-related genes in Changsha County in China and compare the clinical effectiveness of genotype-guided and clinical experience-guided antihypertensive therapy in hypertensive individuals.

Methods: A total of 9,933 essential hypertensive participants from Changsha County were consecutively enrolled in our study, and 7 genetic polymorphic loci (, , , , , and ) were detected by a polymerase chain reaction (PCR)-fluorescence probe.

Downregulation of lncRNA SNHG16 inhibits vascular smooth muscle cell proliferation and migration in cerebral atherosclerosis by targeting the miR-30c-5p/SDC2 axis.

Atherosclerosis (AS) is the basic lesion underlying the occurrence and development of cerebrovascular diseases. Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a crucial role in AS. We aimed to explore the role of SNHG16 in AS and the molecular mechanism of VSMC involvement in the regulation of AS.

TNF-α-Induced NOD2 and RIP2 Contribute to the Up-Regulation of Cytokines Induced by MDP in Monocytic THP-1 Cells.

Nucleotide-binding oligomerization domain containing 2 (NOD2)-induced signal transduction and cytokine production is regulated by a number of factors. However, the feedback effect of the pro-inflammatory TNF-α on NOD2-induced inflammation is not fully understood. In this study, we found unexpectedly that TNF-α up-regulated NOD2 ligand MDP-induced production of the CXC chemokines, including CXCL1, 2, and 8, and the pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, in a dose-dependent manner at both mRNA and protein levels in monocytic THP-1 cells.

[Association of Toll-like receptor 2 and 4 gene polymorphisms with risk of coronary atherosclerotic artery disease in Hunan Han population].

To explore Toll-like receptor 2 (TLR2) and TLR4 polymorphism in Han people from Hunan region and its association with coronary atherosclerotic heart disease.
 Methods: Sanger sequence and statistical analysis were performed to identify the polymorphism of TLR2 and TLR4 genes in 347 unrelated Hunan Han subjects, including 180 healthy people (control group) and 167 patients with coronary atherosclerotic heart disease (coronary atherosclerotic heart disease group).
 Results: There was no significant difference in the genotype frequency and allelic frequency for TLR2 SNP2258G>A and TLR4 SNP896A>G between the 2 groups (P>0.

Transcriptome profile of rat genes in injured spinal cord at different stages by RNA-sequencing.

Background: Spinal cord injury (SCI) results in fatal damage and currently has no effective treatment. The pathological mechanisms of SCI remain unclear. In this study, genome-wide transcriptional profiling of spinal cord samples from injured rats at different time points after SCI was performed by RNA-Sequencing (RNA-Seq).

Temporal kinetics of CD8 CD28 and CD8 CD28 T lymphocytes in the injured rat spinal cord.

This study aims to explore the temporal changes of cytotoxic CD8 CD28 and regulatory CD8 CD28 T-cell subsets in the lesion microenvironment after spinal cord injury (SCI) in rats, by combination of immunohistochemistry (IHC) and flow cytometry (FCM). In the sham-opened spinal cord, few CD8 T cells were found. After SCI, the CD8 T cells were detected at one day post-injury (dpi), then markedly increased and were significantly higher at 3, 7, and 14 dpi compared with one dpi (p < 0.

Co-transplantation of MRF-overexpressing oligodendrocyte precursor cells and Schwann cells promotes recovery in rat after spinal cord injury.

Oligodendrocyte (OL) replacement is a promising treatment strategy for spinal cord injury (SCI). However, the poor survival of transplanted OLs or their precursors and inhibition of axonal regeneration are two major challenges with this approach. Our previous study showed that Schwann cells (SCs) promoted survival, proliferation, and migration of transplanted OL progenitor cells (OPCs) and neurological recovery.

Molecular characterization of a Class I Newcastle disease virus strain isolated from a pigeon in China.

Constant monitoring is performed to elucidate the role of natural hosts in the ecology of Newcastle disease virus (NDV). In this study, an NDV strain isolated from an asymptomatic pigeon was sequenced and analysed. Results showed that the full-length genomes of this isolate were 15,198 nucleotides with the gene order of 3'-NP-P-M-F-HN-L-5'.

Differential effects of myelin basic protein-activated Th1 and Th2 cells on the local immune microenvironment of injured spinal cord.

Myelin basic protein (MBP) activated T cells (MBP-T) play an important role in the damage and repair process of the central nervous system (CNS). However, whether these cells play a beneficial or detrimental role is still a matter of debate. Although some studies showed that MBP-T cells are mainly helper T (Th) cells, their subtypes are still not very clear.

Ghrelin inhibits AngII -induced expression of TNF-α, IL-8, MCP-1 in human umbilical vein endothelial cells.

Aim: Ghrelin, a gastric peptide, is involved in several metabolic and cardiovascular processes. Emerging evidence indicates the potential involvement of ghrelin in low-grade inflammatory diseases such as atherosclerosis and hypertension. Cytokine-induced inflammation is critical in these pathological states.

Relationship between prehypertension and incidence of chronic kidney disease in a general population: a prospective analysis in central south China.

Objective: The objective of the study was to investigate whether prehypertension is associated with progression to chronic kidney disease (CKD) in the general population in central south China.

Methods: A prospective cohort study was carried out in 1,703 white-collar workers without preexisting CKD in Changsha in 2006 at baseline. The cohort population was followed for an average of 54 months by annual examinations.

[Cross-sectional study on high-normal blood pressure and chronic kidney disease in occupational physical examination population in Changsha].

Objective: To investigate the relationship between high-normal blood pressure and chronic kidney disease (CKD) in occupational physical examination population in Changsha.

Methods: With a convenient sampling method, a cross-sectional survey of representative sample of 11 274 white collar workers was conducted in Changsha between March 2011 and May 2011 in a large comprehensive hospital. All subjects were assigned into 4 groups: a normal blood pressure group, a high-normal blood pressure group, an undiagnosed hypertension group, and a diagnosed hypertension group.

The role of profilin-1 in endothelial cell injury induced by advanced glycation end products (AGEs).

Background: Accumulation of advanced glycation end products (AGEs) in the vasculature triggers a series of morphological and functional changes contributing to endothelial hyperpermeability. The reorganisation and redistribution of the cytoskeleton regulated by profilin-1 mediates endothelial cell contraction, which results in vascular hyperpermeability. This study aimed to investigate the pivotal role of profilin-1 in the process of endothelial cell damage induced by AGEs.

Increased platelet volume in a general population with prehypertension: a cross-sectional study of 80 545 participants from China.

Mean platelet volume (MPV), an indicator of platelet activation, has been shown to be elevated in patients with hypertension. However, data available on the association between MPV level and prehypertension are limited. Prehypertension is also associated with an increase in cardiovascular morbidity and mortality.

MDP up-regulates the gene expression of type I interferons in human aortic endothelial cells.

Muramyldipeptide (MDP), the minimum essential structure responsible for the immuno-adjuvant activity of peptidoglycan, is recognized by intracellular nuclear-binding oligomerization domain 2 (NOD2). Here, we obtained evidence that the treatment of human aortic endothelial cells (HAECs) with MDP up-regulated the gene expression of type I interferons in a dose- and time-dependent manner. MDP also up-regulated the expression of the receptor NOD2, suggesting that MDP may induce a positive feedback response.

Extracellular nucleotide inhibits cell proliferation and negatively regulates Toll-like receptor 4 signalling in human progenitor endothelial cells.

Extracellular nucleotides mediate a wide range of physiological effects by interacting with plasma membrane P2 purinergic receptors. P2 receptors are expressed in certain kinds of stem cells, and function to induce cytokine expression and to modulate cell proliferation. We have analysed the expression and the function of P2 receptors in human umbilical cord blood-derived EPCs (endothelial progenitor cells).

The effect of endothelial progenitor cells on angiotensin II-induced proliferation of cultured rat vascular smooth muscle cells.

Previous studies have demonstrated that endothelial progenitor cells (EPCs) could delay the progress of vascular remodeling in blood vessel-proliferating diseases. The proliferation of vascular smooth muscle cells (VSMCs) is a pivotal factor in cardiovascular diseases. In this study, we investigated whether EPCs could inhibit the Angiotensin II (Ang II)-induced proliferation of VSMCs.

The functional expression of TLR3 in EPCs impairs cell proliferation by induction of cell apoptosis and cell cycle progress inhibition.

Toll-like receptor 3 (TLR3), a member of the TLR family that recognizes double-stranded RNA (dsRNA), plays an important role in antiviral immunity. TLR3 is widely expressed in various cells and the activation of TLR3 induces cell apoptosis in some cells. However, the effect of TLR3 on cell proliferation in endothelial progenitor cells (EPCs) is unclear.

Calcitonin gene-related peptide released from endothelial progenitor cells inhibits the proliferation of rat vascular smooth muscle cells induced by angiotensin II.

We have recently demonstrated that endothelial progenitor cells (EPCs) inhibit AngII-induced proliferation of vascular smooth muscle cells (VSMCs) by inactivating MAPKs and NF-κB signaling pathway and reducing expression of oncogene c-myc and c-fos. The inhibitory effect of EPCs on VSMCs is associated with paracrine mechanism. However, the potential mechanism of EPCs on the regulation of AngII-induced proliferation of VSMCs was unknown.

P2Y11 impairs cell proliferation by induction of cell cycle arrest and sensitizes endothelial cells to cisplatin-induced cell death.

Extracellular ATP mediates a wide range of physiological effects, including cell proliferation, differentiation, maturation, and migration. However, the effect of ATP on cell proliferation has been contradictory, and the mechanism is not fully understood. In the current study, we found that extracellular ATP significantly inhibited the proliferation of human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs).

Toll-like receptor 3 (TLR3) induces apoptosis via death receptors and mitochondria by up-regulating the transactivating p63 isoform alpha (TAP63alpha).

Toll-like receptor 3 (TLR3), a member of the pathogen recognition receptors, is widely expressed in various cells and has been shown to activate immune signaling pathways by recognizing viral double-stranded RNA. Recently, it was reported that the activation of TLR3 induced apoptosis in some cells, but the detailed molecular mechanism is not fully understood. In this study, we found that in endothelial cells polyinosinic-polycytidylic acid (poly(I-C)) induced dose- and time-dependent cell apoptosis, which was elicited by TLR3 activation, as TLR3 neutralization and down-regulation repressed the apoptosis.

Effect of ghrelin on angiotensin II induced human umbilicus vein endothelial cell oxidative stress and endothelial cell injury.

Objective: To determine the effect of ghrelin on protecting the human umbilical vein endothelial cells (HUVEC) from injury by angiotensin II (Ang II) in vitro.

Methods: (1) HUVEC was incubated for 24 h with AngII whose final concentration in the medium varied from 10⁻⁹ to 10⁻⁶ mol/L or pretreated with 10⁻⁹ to 10⁻⁶ mol/L ghrelin for 2 h before incubation for 24 h with Ang II whose final concentration in the medium was 10⁻⁶ mol/L. HUVECs were harvested to measure the cell vitality and cell apoptosis.

The expression of functional Toll-like receptor 4 is associated with proliferation and maintenance of stem cell phenotype in endothelial progenitor cells (EPCs).

Endothelial dysfunction is involved in various cardiovascular diseases such as atherosclerosis. Endothelial progenitor cells (EPCs) contribute to re-endothelialization and neo-vascularization, and the increase of EPCs in peripherial circulation benefits the prognosis of cardiovascular disease. However, little is known about the biological stimuli that initiate the proliferation and the maintenance of stem cell phenotype of EPCs.