Abstract
Endothelial progenitor cells (EPCs) are candidates for gene therapies against retinal neovascularization (NV). The aim of present study was to investigate the effects of endostatin transfection on EPC function. In the present study, the EPCs were infected with lentivirus overexpressing endostatin. The transfection effects of endostatin overexpression on the proliferation, migratory, differentiation, apoptosis and the cell cycle of this cell line were determined. The real-time quantitative polymerase chain reaction (RT-qPCR) and western blot assays showed high expression levels of endostatin. A cell counting kit-8 assay showed that endostatin overexpression inhibited EPC proliferation. The transwell assay indicated that endostatin overexpression could suppress EPC migration. Furthermore, endostatin overexpression enhanced apoptosis (as showed by AnnexinV-FITC/propidiumiodide staining analysis), induced differentiation and blocked the cell cycle. As compared with negative control group, EPC viability significantly decreased in gene transfection group. In conclusion, present study determined the feasibility of lentivirus-mediated endostatin gene transfer, and indirectly proved the effect of endostatin secretion on EPCs. Also our study provided a new opportunity for the potential application of gene therapy in retinal NV.
Highlights
Endostatin is a 20 kDa C-terminal fragment of collagen XVIII with antiangiogenic activity
Compared to the negative control (NC) group, the endostatin mRNA levels in the endostatin overexpression (OE) group (EPCs which were transduced with recombinant lentiviral vectors expressing both green fluorescent protein (GFP) and endostatin) were significantly increased (P
Endothelial progenitor cells (EPCs) are cells of mesodermal origin found in the bone marrow, spleen, umbilical cord blood, and peripheral blood [21]
Summary
Endostatin is a 20 kDa C-terminal fragment of collagen XVIII with antiangiogenic activity. It inhibits endothelial cell (EC) proliferation and potently inhibits angiogenesis and tumor growth [1,2]. It was reported that endostatin could offer an innovative pharmaceutical strategy for the prevention of retinal neovascularization (NV) [3]. Endostatin is not stable and its transient effect limits its widespread clinical application. Lentiviral vectors are advantageous and receive much attention due to their stable delivery of the transferred gene into the host cell’s chromosomes [4,5,6]. Gene transfer strategies [712] have the potential to provide sustained, high, local concentrations of antiangiogenic mediators to prevent progression of ocular NV [13,14,15]
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