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.

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.

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.

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.

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.