A simply prepared small-diameter artificial blood vessel that promotes in situ endothelialization.

Synthetic grafts are of limited use in small-diameter vessels (Φ<6mm) due to the poor patency rate. The inability of such grafts to achieve early endothelialization together with the compliance mismatch between the grafts and the native vessels promote thrombosis, which eventually leads to graft occlusion. In the current study, stromal cell-derived factor (SDF)-1α/vascular endothelial growth factor (VEGF)-loaded polyurethane (PU) conduits were simply prepared via electrospinning.

Improving endothelialization by the combined application of polyethylene glycol coated cerium oxide nanoparticles and VEGF in electrospun polyurethane scaffolds.

Synthetic small-diameter vascular grafts are of limited use mainly due to the lack of endothelial cells (ECs), which inhibit intraluminal thrombosis and intimal hyperplasia. Grafts loaded with homing factors for circulating endothelial progenitor cells (EPCs) have the potential to achieve in situ endothelialization. In view of the important role that EPCs play in the construction of small-diameter artificial blood vessels, antioxidant therapy aiming to inhibit oxidative stress-induced EPC apoptosis should be the focus of clinical interest.

Down-regulation of mir-542-3p promotes neointimal formation in the aging rat.

Aim: To explore mir-542-3p mediated inhibition of vascular smooth muscle cell (VSMC) proliferation through the inhibition of Syk activation.

Methods And Results: MicroRNA (mir)-542-3p was selected for analysis based on miRNA microarray and qRT-PCR results. In vitro mir-542-3p expression was significantly downregulated in old (o)VSMCs compared with young (y)VSMCs under serum stimulation conditions.

Hydrogen-rich medium suppresses the generation of reactive oxygen species, elevates the Bcl-2/Bax ratio and inhibits advanced glycation end product-induced apoptosis.

The purpose of the present study was to determine whether using hydrogen-rich medium (HRM) to increase hydrogen levels in endothelial cells (ECs) protects ECs from apoptosis induced by advanced glycation end products (AGEs). The thoracic aorta was removed from 2-3-year-old Sprague-Dawley rats, and ECs were isolated and cultured. After culturing ECs in the presence of AGEs and/or with HRM for 24 h, Annexin V/7-AAD and TUNEL staining were carried out to detect apoptosis.

Hydrogen-rich saline prevents neointima formation after carotid balloon injury by suppressing ROS and the TNF-α/NF-κB pathway.

Background: Reactive oxygen species (ROS) play a pivotal role in neointima hyperplasia after balloon injury. Molecular hydrogen has emerged as a novel antioxidant and has been proven effective in treating many diseases.

Objectives: We aimed to determine the mechanism by which hydrogen affects neointima formation.

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.

Imaging targeted at tumor with (188)Re-labeled VEGF(189) exon 6-encoded peptide and effects of the transfecting truncated KDR gene in tumor-bearing nude mice.

Introduction: Planar imaging of (188)Re-labeled vascular endothelial growth factor (VEGF)(189) exon 6-encoded peptide (QKRKRKKSRYKS) with single photon emission computed tomography (SPECT) in tumor-bearing nude mice and effects of the transfecting truncated KDR gene on its imaging were investigated, so as to provide a basis for further applying the peptide to tumor-targeted radionuclide treatment.

Methods: QKRKRKKSRYKS, coupling with mercaptoacetyltriglycine (MAG(3)) chelator was labeled with (188)Re; then in vivo distribution, planar imaging with SPECT and blocking experiment in tumor-bearing nude mice were analyzed. Recombinant adenovirus vectors carrying the truncated KDR gene were constructed to transfect tumor tissues to evaluate the effects of truncated KDR on the in vivo distribution and tumor planar imaging of (188)Re-MAG(3)-QKRKRKKSRYKS in tumor-bearing nude mice.