KAP1 silencing relieves OxLDL-induced vascular endothelial dysfunction by down-regulating LOX-1
| Autor: | Chang Liang, Suhua Qi, Wan Wang, Wei Zhou, Linyan Huang, Haidi Fan, Ma Ping, Tianqing Yan |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Endothelial nitric oxide synthase (eNOS) Nitric Oxide Synthase Type III Biophysics Down-Regulation Cell Death & Injury Oxidative phosphorylation Tripartite Motif-Containing Protein 28 Biochemistry Cell Line 03 medical and health sciences 0302 clinical medicine Enos Cell Movement medicine Gene silencing Humans Gene Silencing Endothelial dysfunction Phosphorylation Molecular Biology Research Articles Cell Proliferation chemistry.chemical_classification Reactive oxygen species KRAB domain-associated protein 1 (KAP1) Oxidized low-density lipoprotein (OxLDL) biology Cell adhesion molecule Endothelial Cells Cell Biology medicine.disease biology.organism_classification Scavenger Receptors Class E Cell biology Lipoproteins LDL 030104 developmental biology Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) chemistry Cardiovascular System & Vascular Biology 030220 oncology & carcinogenesis Cell Migration Adhesion & Morphology lipids (amino acids peptides and proteins) Endothelial dysfunction (ED) Reactive Oxygen Species Lipoprotein Signal Transduction |
| Zdroj: | Bioscience Reports |
| ISSN: | 1573-4935 0144-8463 |
| Popis: | KRAB domain-associated protein 1 (KAP1) is highly expressed in atherosclerotic plaques. Here, we studied the role of KAP1 in atherosclerosis development using a cell model of endothelial dysfunction induced by oxidative low-density lipoprotein (OxLDL). The phosphorylation and protein levels of KAP1 were similar between OxLDL-treated and non-treated endothelial cells (ECs). KAP1 depletion significantly inhibited the production of OxLDL-enhanced reactive oxygen species and the expression of adhesion molecules in ECs. Treatment with OxLDL promoted the proliferation and migration of ECs, which was also confirmed by the elevated levels of the proliferative markers c-Myc and PCNA, as well as the migratory marker MMP-9. However, these effects were also abrogated by KAP1 depletion. Moreover, the depletion of KAP1 in OxLDL-treated ECs resulted in decreases in the LOX-1 level and increases in eNOS expression. Generally, the data suggest that strategies targeting KAP1 depletion might be particularly useful for the prevention or treatment of atherosclerosis. |
| Databáze: | OpenAIRE |
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