ArticleAnimal models and experimental medicine2026
The HCMV-encoded miR-UL36-3p promotes angiogenesis of endothelial cells by downregulating FOXO3.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHuman cytomegalovirus (HCMV) infection is related to the acceleration of transplant vascular sclerosis, atherosclerosis, and coronary restenosis. A shared theme of these vascular illnesses is pathologic angiogenesis. Nevertheless, how HCMV infection causes angiogenesis is not fully understood. Human serum contains HCMV-encoded miRNAs, and it is unclear whether these virus-derived miRNAs can regulate angiogenesis. This research looks into HCMV-encoded miRNA's role in angiogenesis of endothelial cells.
methodsEndothelial cell proliferation was examined by CCK8 assay, and cell migration capability was established using a Transwell Boyden Chamber. Western blotting alongside luciferase reporter assay verified the direct regulation of FOXO3 by HCMV-encoded miRNAs, including hcmv-miR-UL36-3p. hcmv-miR-UL36-3p's pro-angiogenic action was examined by angiogenesis assays (in vivo) and capillary tube formation (in vitro), which were performed by giving C57BL/6J mice subcutaneous Matrigel injections containing bFGF along with simultaneous injections of either hcmv-miR-UL36-3p or ncRNA once every 4 days. After 8 days, Matrigel plugs were examined.
resultshcmv-miR-UL36-3p was upregulated in patients with atherosclerosis. Overexpression of hcmv-miR-UL36-3p enhanced capillary tube development, motility, and proliferation in endothelial cells. hcmv-miR-UL36-3p promoted endothelial cell tube formation through directly binding to and downregulating FOXO3. Experiments in mice further confirmed that hcmv-miR-UL36-3p promoted angiogenesis in vivo.
conclusionsThe HCMV-encoded miR-UL36-3p can trigger angiogenesis in endothelial cells by targeting FOXO3. Our work provides a conceivable mechanism of how HCMV-encoded miRNAs contribute to vascular illness.
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