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Lookup NU author(s): Dr Naomi Willis
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Human endothelial progenitor cells (hEPC) are adult stem cells located in the bone marrow and peripheral blood. Studies have indicated that hEPC play an important role in the recovery and repair of injured endothelium, however, their quantity and functional capacity is reduced in several diseases including hypercholesterolemia. Recently, it has been demonstrated that hEPC express lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and its activation by oxidized low-density lipoprotein (ox-LDL) induces cellular dysfunction and apoptosis. This study aimed to investigate whether overexpression of LOXIN, a truncated isoform of LOX-1 that acts as a dominant negative, plays a protective role against ox-LDL-induced apoptosis in hEPC. Human endothelial progenitor cells exposed to ox-LDL showed a significant increase in LOX-1 expression, and apoptosis began at ox-LDL concentrations above 50 g/mL. All hEPC apoptosed at 200 g/mL ox-LDL. High LOXIN expression was generated using adenoviral systems in hEPC and SiHa cells transduced with 100 colony-forming units per cell. Transduced LOXIN localized to the plasma membrane and blocked ox-LDL uptake mediated by LOX-1. Overexpression of LOXIN protected hEPC from ox-LDL-induced apoptosis, and therefore maybe a novel way of improving hEPC function and quantity. These results suggest that adenoviral vectors of LOXIN may provide a possible treatment for diseases related to ox-LDL and vascular endothelium dysfunction, including atherosclerosis.
Author(s): Veas C, Jara C, Willis ND, Perez-Contreras K, Gutierrez N, Toledo J, Fernandez P, Radojkovic C, Zuniga FA, Escudero C, Aguayo C
Publication type: Article
Publication status: Published
Journal: Journal of Cardiovascular Pharmacology
Year: 2016
Volume: 67
Issue: 4
Pages: 326-335
Print publication date: 01/04/2016
Acceptance date: 01/01/1900
ISSN (print): 0160-2446
ISSN (electronic): 1533-4023
Publisher: Lippincott Williams & Wilkins, Ltd.
URL: http://dx.doi.org/10.1097/FJC.0000000000000358
DOI: 10.1097/FJC.0000000000000358
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