ArticleMolecular medicine reports2018
Generation of an anti-angiogenic endothelial progenitor cell line via endostatin gene transfer.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Endostatin-based anti-angiogenic therapy and immune modulation: mechanisms and synergistic potential in cancer treatment.Frontiers in immunology · 2025Review
- Vascular Remodeling in Moyamoya Angiopathy: From Peripheral Blood Mononuclear Cells to Endothelial Cells.International journal of molecular sciences · 2020Article
- An Endostatin-lentivirus (ES-LV)-EPC gene therapy agent for suppression of neovascularization in oxygen-induced retinopathy rat model.BMC molecular and cell biology · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The viability of endothelial progenitor cells (EPCs) as a therapeutic treatment for neovascularization (NV) was subject to investigation in the present study. Furthermore, endostatin has previously been demonstrated to be an inhibitor of angiogenesis and a suppressant of vascular leakage. The aim of the present study was to generate transgenic EPCs with anti‑angiogenic effects for the treatment of ocular NV. EPCs were obtained from rat peripheral blood samples and then verified. A lentiviral‑endostatin‑green fluorescent protein recombinant construct was generated and used to infect EPCs. Transfected cells were then subjected to puromycin selection. Reverse transcription‑quantitative polymerase chain reaction and a western blot assay were then applied in order to determine both the endostatin mRNA and protein expression levels, respectively. In addition, vascular endothelial growth factor (VEGF) expression levels were also detected in order to observe the anti‑angiogenic effect of the endostatin‑transfected EPCs. Following puromycin (1 µg/ml) selection for 4 days, a stable endostatin‑transfected EPC line was generated. In this stable endostatin-transfected EPC line, the expression levels of endostatin increased; whereas the expression levels of VEGF decreased. The results of the present study revealed that EPCs can be genetically modified to overexpress endostatin, which may provide the cells with an anti‑angiogenic effect via increased expression of endostatin and decreased expression of VEGF. Thus, EPCs genetically modified to overexpress endostatin may serve as a potential therapeutic agent for ocular NV treatment.
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