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Interleukin-1β Promotes Ox-LDL Uptake by Human Glomerular Mesangial Cells via LOX-1

The aim of this study was to determine whether interleukin-1β (IL-1β) promotes oxidised low-density lipoprotein (Ox-LDL) uptake by human glomerular mesangial cells (HMCs) and its effect on the expression of lectin-like Ox-LDL receptor 1 (LOX-1) and to identify pathways through which IL-1β affects li...

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Detalles Bibliográficos
Autores principales: Liu, Hua, Li, Yinping, Lin, Na, Dong, Xingtong, Li, Wen, Deng, Yinghui, Ma, Lina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211151/
https://www.ncbi.nlm.nih.gov/pubmed/32410835
http://dx.doi.org/10.7150/ijms.43981
Descripción
Sumario:The aim of this study was to determine whether interleukin-1β (IL-1β) promotes oxidised low-density lipoprotein (Ox-LDL) uptake by human glomerular mesangial cells (HMCs) and its effect on the expression of lectin-like Ox-LDL receptor 1 (LOX-1) and to identify pathways through which IL-1β affects lipid uptake. Confocal laser scanning microscopy and flow cytometry were used to observe the effect of IL-1β on lipid uptake by HMCs and the pathway by which IL-1β may mediate lipid uptake. Real-time polymerase chain reaction (PCR) and western blotting were used to evaluate the effect of IL-1β on LOX-1 expression. Confocal laser scanning microscopy and flow cytometry revealed that IL-1β promoted uptake of fluorescent Dil-labelled Ox-LDL(Dil-Ox-LDL) by HMCs and the enhanced uptake of Dil-Ox-LDL was partially inhibited by an anti-LOX-1 antibody evaluated by flow cytometry. Further, IL-1β promoted LOX-1 mRNA and protein expression of HMCs in a dose- and time-dependent manner. Thus, Ox-LDL is ingested by HMCs under basic conditions. Inflammatory cytokine IL-1β promotes Ox-LDL uptake by HMCs. Furthermore, IL-1β promotes the mRNA and protein expression of LOX-1, a specific receptor of Ox-LDL, suggesting that the enhancement of Ox-LDL uptake may be mediated by LOX-1 pathway. Anti-LOX-1 therapy may be a promising option for treatment of glomerulosclerosis.