LOX-1 deficient mice show resistance to zymosan-induced arthritis

Hashimoto, Kazuhiko; Oda, Yutaka; Nakagawa, Kōichi; Ikeda, Tatsuya; Ohtani, Kazuhiro; Akagi, Masao

doi:10.4081/ejh.2018.2847

Cited by 11 publications

(6 citation statements)

References 35 publications

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“…60 Therefore, in vitro and in vivo studies indicate involvement of the LOX-1/ox-LDL system in OA. Recently, Xinhua et al 61 showed possible involvement of the LOX-1/ox-LDL system in pathogenesis and progression of human intervertebral disc degeneration or herniation. These results indicate that the LOX-1/ox-LDL system is strongly involved in the pathogenesis of OA (Table 1, Figure 1).…”

Section: Evidence For Involvement Of Lox-1/ox-ldl In Oamentioning

confidence: 99%

The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review

Hashimoto

Akagi

2020

J Int Med Res

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Osteoarthritis (OA) is a chronic joint disorder that causes degeneration of cartilage, synovial inflammation, and formation of osteophytes. Aging, obesity, and sex are considered the main risk factors of OA. Recent studies have suggested that metabolic syndrome (MetS) disorders, such as hypertension, hyperlipidemia, diabetes mellitus, and obesity, may be involved in the pathogenesis and progression of OA. MetS disorders are common diseases that also result in atherosclerosis. Researchers believe that OA and atherosclerosis have underlying similar molecular mechanisms because the prevalence of both diseases increases with age. Oxidation of low-density lipoprotein (ox-LDL) is believed to play a role in the pathogenesis of atherosclerosis. Recent reports have shown that ox-LDL and low-density lipoprotein receptor 1 (LOX-1) are involved in the pathogenesis of OA. The purpose of this narrative review is to summarize the current understanding of the role of the LOX-1/ox-LDL system in the pathogenesis of OA and to reveal common underlying molecular pathways that are shared by MetS in OA and the LOX-1/ox-LDL system.

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Section: Evidence For Involvement Of Lox-1/ox-ldl In Oamentioning

confidence: 99%

The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review

Hashimoto

Akagi

2020

J Int Med Res

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“…International Publisher of LOX-1/Ox-LDL system may be involved in the pathogenesis of arthritis by using LOX-1 knockout mice, additionally, LOX-1-positive synovial cells and chondrocytes may be potential therapeutic targets for arthritis prevention [8].The current review on regulation, signaling and various effects of LOX-1 has indicated the key contribution of LOX-1 to the atherogenic process. Anti-LOX-1 therapy has been shown to decrease inflammation, oxidative stress and atherosclerosis, making LOX-1 a promising target of therapy for atherosclerosis and related disorders [9].…”

Section: Ivyspringmentioning

confidence: 99%

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

Liu

Lin

et al. 2020

Int. J. Med. Sci.

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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.

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“…Previous studies have shown that LOX-1 knockout or LOX-1 blocking antibodies can inhibit the inflammatory response (Hashimoto et al, 2018), lipid deposition (Mehta et al, 2007), and apoptosis (Pirillo et al, 2013;Schaeffer et al, 2009) induced by Ox-LDL. As HNG restrained LOX-1 content induced by Ox-LDL, it is uncertain whether the role of reducing lipid accumulation is mediated through the inhibition of LOX-1 expression.…”

Section: Lox-1 Knockdown Inhibits the Effect Of Hng On Reducing Accummentioning

confidence: 99%

[Gly14]‐Humanin Prevents Lipid Deposition and Endothelial Cell Apoptosis in a Lectin‐like Oxidized Low‐density Lipoprotein Receptor‐1‐Dependent Manner

Ding

Feng

Zhu

et al. 2019

Lipids

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Oxidized low‐density lipoprotein (Ox‐LDL) may induce apoptosis and dysfunction of vascular endothelial cells, contributing to the initiation and development of atherosclerosis and lectin‐like oxidized low‐density lipoprotein receptor‐1 (LOX‐1) plays a central role in Ox‐LDL uptake in the course of atherogenesis. Humanin (HN), a mitochondrial‐derived peptide, was recently demonstrated to exert a protective role against endothelial dysfunction and Ox‐LDL‐induced progression of atherosclerosis. The HN analog HNGF6A (HNG) modulates cholesterol metabolism in macrophage RAW 264.7 cells. However, whether HNG affects Ox‐LDL metabolism in endothelial cells is unknown. In this study, we investigated the effect of HNG on Ox‐LDL accumulation in human umbilical vein endothelial cell (HUVEC) and its underlying mechanisms. HUVEC were preincubated with HNG for 1 h before addition of Ox‐LDL. Total cholesterol content was measured by using a tissue total cholesterol assay kit and flow cytometry. Cell viability was measured by CCK8 assay. Protein content was examined by Western blot assays. Flow cytometry was used to identify apoptotic cells. Flow cytometry and tissue total cholesterol assays showed that HNG reduced Ox‐LDL accumulation in HUVEC. In addition, HNG inhibited Ox‐LDL‐induced apoptosis of HUVEC. Western blot results showed that HNG reduced LOX‐1 protein content. However, when LOX‐1 was knocked down or inhibited, the effect of HNG in reducing Ox‐LDL aggregation and apoptosis in HUVEC disappeared. Our study demonstrated that HNG reduces lipid aggregation and apoptosis in HUVEC in a LOX‐1‐dependent manner.

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LOX-1 deficient mice show resistance to zymosan-induced arthritis

Cited by 11 publications

References 35 publications

The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review

The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review

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

[Gly14]‐Humanin Prevents Lipid Deposition and Endothelial Cell Apoptosis in a Lectin‐like Oxidized Low‐density Lipoprotein Receptor‐1‐Dependent Manner

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