Identification of crucial genes that induce coronary atherosclerosis through endothelial cell dysfunction in AMI-identifying hub genes by WGCNA.

Objective: To identify the most relevant genes of cardiovascular disease in acute myocardial infarction patients using weighted gene co-expression network analysis (WGCNA).

Methods: The microarray dataset of GSE66360 was downloaded from the Gene Expression Omnibus (GEO) website. The differential genes with adjusted P < 0.

Study of the Phase-Change Thermal-Storage Characteristics of a Solar Collector.

A combined solar phase-change thermal-storage heating system is proposed, wherein erythritol is used as the phase-change material (PCM) used to fill the thermal-storage device, and the storage cavity is heated and stored with a disc concentrator. The Solidification/Melting, Volume-of-Fluid (VOF) model of ANSYS Fluent software was used to simulate the phase-change process of erythritol inside the thermal-storage device. The thermal-storage device was designed based on our numerical calculations, and its performance was tested.

Endothelial progenitor cells and coronary artery disease: Current concepts and future research directions.

Vascular injury is a frequent pathology in coronary artery disease. To repair the vasculature, scientists have found that endothelial progenitor cells (EPCs) have excellent properties associated with angiogenesis. Over time, research on EPCs has made encouraging progress regardless of pathology or clinical technology.

Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice.

This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We established an atherosclerosis mouse model in ApoE knockout mice, followed by gain- and loss-of-function approaches. H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1.

Magnetic Resonance Imaging and Biomechanical Analysis of Adipose-derived Stromal Vascular Fraction Applied on Rotator Cuff Repair in Rabbits.

Background: Adipose-derived stromal vascular fraction (ADSVF) can be applied to repair tendon and ligament tears. ADSVF treatment has a better therapeutic potential than adipose stem cells alone in promoting the healing of connective tissue injury in rabbit models. Magnetic resonance imaging (MRI) and biomechanical testing were used in this study to evaluate the efficiency of SVF in the healing of tendon-bone interface of a rotator cuff injury after reattachment.

[Slfn1 inhibited the migration of endothelial progenitor cells in vitro].

Objective: To explore the effect of Schlafen 1 (Slfn1) on the migration of endothelial progenitor cells (EPCs).

Methods: Rat bone marrow derived EPCs were isolated and cultured. Ad-Slfn1, ShRNA-Slfn1, ShRNA-control and Ad-control were transfected into EPCs respectively.

Schlafen 1 inhibits the proliferation and tube formation of endothelial progenitor cells.

Endothelial progenitor cells (EPCs) are the major source of cells that restore the endothelium during reendothelialization. This study was designed to investigate whether Schlafen 1 (Slfn1) has an effect on the proliferation and tube formation of EPCs in vivo. Slfn1 was expressed in rat EPCs.

Overexpression of SDF-1α enhanced migration and engraftment of cardiac stem cells and reduced infarcted size via CXCR4/PI3K pathway.

Cardiac stem cells (CSCs) can home to the infarcted area and regenerate myocardium. Stromal cell-derived factor-1α/C-X-C chemokine receptor type 4 (SDF-1α/CXCR4) axis is pivotal in inducing CSCs migration. However, the mechanisms remain unclear.

An essential role for the Id1/PI3K/Akt/NFkB/survivin signalling pathway in promoting the proliferation of endothelial progenitor cells in vitro.

The enhancement of re-endothelialisation is a critical therapeutic option for repairing injured blood vessels. Endothelial progenitor cells (EPCs) are the major source of cells that participate in endothelium repair and contribute to re-endothelialisation by reducing neointima formation after vascular injury. The over-expression of the inhibitor of differentiation or DNA binding 1 (Id1) significantly improved EPC proliferation.

[Impact of stromal interaction molecule 1 silencing on cell cycle of endothelial progenitor cells].

Objective: To investigate the effect of stromal interaction molecule 1 (STIM1) silencing on EPCs cell cycle.

Methods: Rat bone marrow derived endothelial progenitor cells (EPCs) were isolated and cultured in L-DMEM with 20% FBS. Ad-si/rSTIM1 and Ad-hSTIM1 were then transfected into EPCs and the expression of STIM1 mRNA was detected by RT-PCR.

Aging reduces susceptibility of vascular smooth muscle cells to H₂O₂-induced apoptosis through the down-regulation of Jagged1 expression in endothelial cells.

In addition to excessive proliferation, reduced apoptosis of vascular smooth muscle cells (VSMCs) plays a key role in aging-exaggerated neointima formation after vascular injury. Our previous studies have shown that impaired expression of Jagged1 in the endothelium may be a key event that leads to enhanced VSMC proliferation in the elderly. Here, we are the first to investigate whether the expression of Jagged1 in endothelial cells (ECs) may regulate apoptosis of VSMCs.

Knockdown of transient receptor potential canonical-1 reduces the proliferation and migration of endothelial progenitor cells.

Endothelial progenitor cells (EPCs) play an important role in accelerating endothelial repair after vascular injury. The proliferation and migration of EPCs is a critical first step in restoring endothelial. However, mechanisms for modulating EPC proliferation and migration are still being elucidated.

CCN1 promotes the differentiation of endothelial progenitor cells and reendothelialization in the early phase after vascular injury.

Endothelial progenitor cells (EPCs) contribute to the process of reendothelialization and prevent neointimal formation after vascular injury. The present study was designed to investigate whether the cysteine-rich 61 (CYR61, CCN1), an important matricellular component of local vascular microenvironment, has effect on EPCs differentiation and reendothelialization in response to vascular injury in rat. Following balloon injury, CCN1 was rapidly induced and dynamically changed at vascular lesions.

Silencing stromal interaction molecule 1 by RNA interference inhibits the proliferation and migration of endothelial progenitor cells.

Knockdown of stromal interaction molecule 1 (STIM1) significantly suppresses neointima hyperplasia after vascular injury. Endothelial progenitor cells (EPCs) are the major source of cells that respond to endothelium repair and contribute to re-endothelialization by reducing neointima formation after vascular injury. We hypothesized that the effect of STIM1 on neointima hyperplasia inhibition is mediated through its effect on the biological properties of EPCs.