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Oxidized low-density lipoprotein decreases VEGFR2 expression in HUVECs and impairs angiogenesis.
- Source :
-
Experimental & Therapeutic Medicine . Dec2016, Vol. 12 Issue 6, p3742-3748. 7p. - Publication Year :
- 2016
-
Abstract
- Atherosclerosis (AS), which is triggered by endothelial cell injury, evolves into a chronic inflammatory disease. Oxidized low-density lipoprotein (ox-LDL) is an important risk factor for the development of atherosclerosis; ox-LDL induces atherosclerotic plaque formation via scavenging receptors. The present study used ox-LDL-treated human umbilical vein endothelial cells (HUVECs) to investigate the effect of ox-LDL on angiogenesis. ox-LDL decreased HUVEC proliferation by MTT, induced apoptosis by Annexin V-fluorescein isothiocyanate (FITC) staining and markedly suppressed HUVEC tube formation by the Matrigel assay in a dose-dependent manner. Angiogenesis has been correlated with monocyte invasion, plaque instability and atherosclerotic lesion formation. In addition, ox-LDL induced the overproduction of reactive oxygen species using DCFH-DA staining and increased caspase-3 activity. Vascular endothelial growth factor receptor 2 (VEGFR2) were detected by quantitative polymerase chain reaction and western blot analysis and has previously been observed to have a key role in angiogenesis. Furthermore, the present study demonstrated that the abundance of VEGFR2 was decreased in ox-LDL-treated HUVECs. These results suggested that ox-LDL impairs angiogenesis via VEGFR2 degradation, thus suggesting that VEGFR2 may be involved in adaptation to oxidative stress and AS. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 17920981
- Volume :
- 12
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Experimental & Therapeutic Medicine
- Publication Type :
- Academic Journal
- Accession number :
- 119723446
- Full Text :
- https://doi.org/10.3892/etm.2016.3823