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#31746956   2019/11/20 To Up

Association Between Soluble Lectinlike Oxidized Low-Density Lipoprotein Receptor-1 and Coronary Artery Disease in Psoriasis.

Psoriasis, a chronic inflammatory skin disease associated with accelerated noncalcified coronary burden (NCB) by coronary computed tomography angiography (CCTA), accelerates lipoprotein oxidation in the form of oxidized modified lipoproteins. A transmembrane scavenger receptor for these oxidized modified lipoproteins is lectinlike oxidized low-density lipoprotein receptor-1 (LOX-1), which has been reported to be associated with coronary artery disease. It is unknown whether this receptor is associated with coronary artery disease in psoriasis.
Amit K Dey, Ranjitha Gaddipati, Youssef A Elnabawi, Emily Ongstad, Aditya Goyal, Jonathan H Chung, Heather L Teague, Justin A Rodante, Aparna A Sajja, Alexander V Sorokin, Sundus S Lateef, Milena Aksentijevich, Harry Choi, Aarthi S Reddy, Nevin J Varghese, Jacob Groenendyk, Agastya D Belur, Leonard Genovese, Joshua P Rivers, Joseph Lerman, Mohammad Tarek Kabbany, Charlotte Harrington, Jenis Ortiz, Noor Khalil, Andrew Keel, Yvonne Baumer, Marcus Y Chen, David A Bluemke, Aditya A Joshi, Mariana J Kaplan, Alan T Remaley, Martin P Playford, Sotirios K Karathanasis, Joel M Gelfand, Ruchi Gupta, Nehal N Mehta

1726 related Products with: Association Between Soluble Lectinlike Oxidized Low-Density Lipoprotein Receptor-1 and Coronary Artery Disease in Psoriasis.

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#31746382   2019/11/06 To Up

Dioscin attenuates oxLDL uptake and the inflammatory reaction of dendritic cells under high glucose conditions by blocking p38 MAPK.

Dioscin has been shown to affect the regulation of metabolic diseases, including diabetes; however, the mechanism of action is still unclear. Under high glucose (HG) conditions, the expression of scavenger receptors and the uptake of oxidized low‑density lipoprotein (oxLDL) are upregulated in dendritic cells (DCs), which are critical steps in atherogenesis and inflammation. In this study, the focus was on the impact of dioscin on the function of DCs. Immature DCs were cultured with: 5.5 mM glucose medium (control group); 30 mM glucose medium (HG group); HG + 10 mM dioscin; HG + 20 mM dioscin; HG + 30 mM dioscin; and HG + 40 mM dioscin. For subsequent experiments, 30 mM dioscin was used as the experimental concentration. Dichlorodihydrofluorescein fluorescence was used to measure the intracellular production of reactive oxygen species (ROS) in DCs. The expression levels of the scavenger receptors, including class A scavenger receptors (SR‑A), CD36 and lectin‑like oxidized low‑density lipoprotein receptor‑1 (LOX‑1) were determined via quantitative PCR. The protein expression of p38 mitogen‑activated protein kinase (MAPK) was determined by western blotting. Furthermore, ELISA was used to detect the levels of interleukin (IL)‑6, IL‑10 and IL‑12. Finally, DCs were incubated with diOlistic (Dil)‑labeled oxLDL, and flow cytometry analysis was used to investigate the Dil‑oxLDL‑incorporated fraction. The incubation of DCs with dioscin inhibited the induction of ROS production, in a dose‑dependent manner, under HG conditions. The upregulation of SR‑A, CD36 and LOX‑1 genes was partially abolished by dioscin, which also partially reversed p38 MAPK protein upregulation. Furthermore, increased secretion of IL‑6 and IL‑12, and decreased secretion of IL‑10 in DCs, induced by HG, was also reversed by dioscin. To conclude, dioscin could attenuate the production of ROS, inflammatory cytokine secretion and oxLDL uptake by DCs in HG conditions by preventing the expression of scavenger receptors and p38 MAPK, thus playing a positive role in preventing atherogenesis.
Ying Li, Yong Li, Te Yang, Ming Wang

2848 related Products with: Dioscin attenuates oxLDL uptake and the inflammatory reaction of dendritic cells under high glucose conditions by blocking p38 MAPK.

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#30744454   // To Up

High Levels of Soluble Lectinlike Oxidized Low-Density Lipoprotein Receptor-1 Are Associated With Carotid Plaque Inflammation and Increased Risk of Ischemic Stroke.

Background When the lectinlike oxidized low-density lipoprotein (ox LDL) receptor-1 ( LOX -1), a scavenger receptor for ox LDL , binds ox LDL , processes leading to endothelial dysfunction and inflammation are promoted. We aimed to study release mechanisms of LOX -1 and how circulating levels of soluble LOX -1 ( sLOX -1) relate to plaque inflammation and future risk for ischemic stroke. Methods and Results Endothelial cells and leukocytes were used to study release of sLOX -1. Plasma levels of sLOX -1 were determined in 4703 participants in the Malmö Diet and Cancer cohort. Incidence of ischemic stroke was monitored. For 202 patients undergoing carotid endarterectomy, levels of sLOX -1 were analyzed in plasma and plaque homogenates and related to plaque inflammation factors. Endothelial cells released sLOX -1 when exposed to ox LDL . A total of 257 subjects experienced stroke during a mean follow-up of 16.5 years. Subjects in the highest tertile of sLOX -1 had a stroke hazard ratio of 1.75 (95% CI, 1.28-2.39) compared with those in the lowest tertile after adjusting for age and sex. The patients undergoing carotid endarterectomy had a significant association between plasma sLOX -1 and the plaque content of sLOX -1 ( r=0.209, P=0.004). Plaques with high levels of sLOX -1 had more ox LDL , proinflammatory cytokines, and matrix metalloproteinases. Conclusions Our findings demonstrate that ox LDL induces the release of sLOX -1 from endothelial cells and that circulating levels of sLOX -1 correlate with carotid plaque inflammation and risk for ischemic stroke. These observations provide clinical support to experimental studies implicating LOX -1 in atherosclerosis and its possible role as target for cardiovascular intervention.
Hanna Markstad, Andreas Edsfeldt, Ingrid Yao Mattison, Eva Bengtsson, Pratibha Singh, Michele Cavalera, Giuseppe Asciutto, Harry Björkbacka, Gunilla Nordin Fredrikson, Nuno Dias, Petr Volkov, Marju Orho-Melander, Jan Nilsson, Gunnar Engström, Isabel Gonçalves

1899 related Products with: High Levels of Soluble Lectinlike Oxidized Low-Density Lipoprotein Receptor-1 Are Associated With Carotid Plaque Inflammation and Increased Risk of Ischemic Stroke.

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#30483757   2018/11/26 To Up

OxLDL promotes lymphangiogenesis and lymphatic metastasis in gastric cancer by upregulating VEGF‑C expression and secretion.

Gastric cancer is one of the most malignant tumor types, and its metastasis is a notable cause of mortality. Among the methods of tumor metastasis, lymphatic metastasis is the predominant one in gastric cancer. A previous study reported that the plasma oxidized low‑density lipoprotein (oxLDL) is the risk factor associated with the development of tumors in patients with abnormal lipid metabolism, but the influence of plasma oxLDL in the lymphatic metastasis of gastric cancer remains unclear. In the present study, the concentration of plasma oxLDL from patients with gastric cancer was detected with an ELISA kit, and the lymphatic vessel density in gastric cancer tissues was determined by D2‑40 staining. The correlation analysis of oxLDL concentration and lymphatic vessel density demonstrated that plasma oxLDL was positively correlated with lymphatic metastasis in patients with gastric cancer. Subsequently, the popliteal lymph node metastasis animal experiment with nude mice confirmed that oxLDL could promote the lymphatic metastasis of gastric cancer. Following this, the western blotting and ELISA data demonstrated that oxLDL promoted the expression and secretion of vascular endothelia growth factor (VEGF)‑C in gastric cancer cell lines. Finally, blocking the lectin‑like oxLDL‑1 (LOX‑1) receptor, a specific receptor for oxLDL, and the nuclear factor (NF)‑κB signaling pathway following oxLDL (50 µg/ml) treatment in HGC‑27 cells revealed that oxLDL could activate the NF‑κB signaling pathway mediated by LOX‑1, with subsequent upregulation of VEGF‑C expression, and secretion in and from gastric cancer cells, and finally that it could promote the lymphatic metastasis of gastric cancer. These data indicate the association between the plasma oxLDL and the lymphatic metastasis of gastric cancer, and indicate that oxLDL elimination may be a potential therapeutic target for the prevention and intervention of early lymph node metastasis in gastric cancer.
Caiqi Ma, Jinye Xie, Chuanghua Luo, Haofan Yin, Ruopu Li, Xi Wang, Wenjun Xiong, Ting Zhang, Ping Jiang, Weiwei Qi, Ti Zhou, Zhonghan Yang, Wei Wang, Jianxing Ma, Guoquan Gao, Xia Yang

1924 related Products with: OxLDL promotes lymphangiogenesis and lymphatic metastasis in gastric cancer by upregulating VEGF‑C expression and secretion.



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#29393358   2018/01/23 To Up

MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism.

Endothelial senescence leads to cell dysfunction, which in turn eventually results in cardiovascular disease. Identifying factors that regulate endothelial senescence may provide insight into the pathogenesis of aging. Insulin-like growth factor (IGF) signaling has a significant role in the physiology of endothelial cells (ECs). Overactivation of IGF signaling has been implicated in promoting the aging process. Lectin‑like oxidized low‑density lipoprotein (oxLDL) receptor‑1 (LOX‑1) is a scavenger receptor that mediates the internalization of oxLDL into cells. Previous studies by our group have indicated that microRNA let‑7g exerts an anti‑aging effect on ECs and also suppresses LOX-1 expression. Since LOX‑1 also induces the aging process, the present study we explored whether let‑7g still exerts an anti‑aging effect on ECs when LOX‑1 is suppressed. Angiotensin II (Ang II) was used to induce senescence in ECs. It was revealed that Ang II significantly increased the expression of aging markers, including β‑galactosidase, LOX‑1, IGF1 and its receptor IGF1R. On the contrary, Ang II decreased the expression of the anti‑aging gene sirtuin 1 (SIRT1). When LOX‑1 was knocked down by small interfering RNA, let‑7g still dose‑dependently decreased the expression of β‑galactosidase (β‑gal), LOX‑1, IGF1 and IGF1R, and SIRT1 was still upregulated. Using senescence‑associated β‑gal staining, it was confirmed that let‑7g exerts a LOX‑1‑independent anti‑aging effect on ECs. In conclusion, the present study demonstrated that let‑7g has an anti‑aging effect regardless of the presence or absence of LOX-1.
Po-Yuan Hsu, Wen-Yi Lin, Ruey-Tay Lin, Suh-Hang H Juo

2374 related Products with: MicroRNA let-7g inhibits angiotensin II-induced endothelial senescence via the LOX-1-independent mechanism.

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#29115480   2017/11/02 To Up

Protective effects of probucol on Ox-LDL-induced epithelial-mesenchymal transition in human renal proximal tubular epithelial cells via LOX‑1/ROS/MAPK signaling.

Oxidized low-density lipoprotein (Ox-LDL), as a strong oxidant, results in renal injury through multiple mechanisms. The aim of the present study was to determine the injury effects of Ox‑LDL and the potential protective effects of the antioxidant reagent probucol on epithelial‑mesenchymal transition (EMT) in human renal proximal tubular epithelial cells (HK‑2) and to further explore the role and interrelation of lectin‑like oxidized low‑density lipoprotein receptor‑1 (LOX‑1), reactive oxygen species (ROS) and mitogen‑activated protein kinase (MAPK) pathway. In the present study, concentrations of 0‑100 µg/ml Ox‑LDL were used to induce HK‑2 cell EMT. Then, probucol (20 µmol/l) and the LOX‑1 inhibitor, polyinosinic acid (250 µg/ml), were also used to pretreat HK‑2 cells. Intracellular ROS activity was evaluated using the specific probe 2',7'‑dichlorodihydrofluorescein diacetate (DCFH‑DA). Concentration of nitric oxide (NO) was determined using a biochemical colorimetric method. Expression of E‑cadherin, α‑smooth muscle actin (SMA), LOX‑1, NADPH oxidase 4 (NOX4), cytochrome b‑245 α chain (p22phox), extracellular signal‑regulated kinase (ERK), and p38 MAPK protein levels were examined by western blotting. The results revealed that Ox‑LDL induced the expression of LOX‑1 and α‑SMA and reduced the expression of E‑cadherin in a dose‑dependent manner, and these effects were inhibited by polyinosinic acid or probucol pretreatment. Stimulation with 50 µg/ml Ox‑LDL induced the expression of NOX4 and p22phox and increased intracellular ROS activity, but NO production in the cell supernatants was not affected. The Ox‑LDL‑mediated increases in Nox4 and p22phox expression and in ROS activity were inhibited by probucol pretreatment. Further investigations into the underlying molecular pathways demonstrated that ERK and p38 MAPK were activated by Ox‑LDL stimulation and then inhibited by probucol pretreatment. The findings of the present study therefore suggest that Ox‑LDL induced EMT in HK‑2 cells, the mechanism of which may be associated with LOX‑1‑related oxidative stress via the ERK and p38 MAPK pathways. Notably, pretreatment with probucol inhibited the Ox‑LDL‑induced oxidative stress by reducing the expression of LOX‑1, and blocked the progression of EMT.
Bing Bing Zhu, Hao Wang, Yang Feng Chi, Yun Man Wang, Xing Mei Yao, Shuang Liu, Huiling Qiu, Ji Fang, Pei Hao Yin, Xue Mei Zhang, Wen Peng

2747 related Products with: Protective effects of probucol on Ox-LDL-induced epithelial-mesenchymal transition in human renal proximal tubular epithelial cells via LOX‑1/ROS/MAPK signaling.

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#29039543   2017/10/13 To Up

Oxidized low density lipoprotein facilitates tumor necrosis factor‑α mediated chondrocyte death via autophagy pathway.

We aimed to investigate the role of oxidized low density lipoprotein (ox‑LDL) in tumor necrosis factor‑α (TNF‑α) mediated chondrocyte death and explore the mechanisms. Ten osteoarthritis (OA) and normal control cartilage tissue and synovial fluid (SF) samples were collected, and the expression of lectin‑like ox‑LDL receptor‑1 (LOX‑1) and ox‑LDL level was examined by real time quantitative PCR and enzyme‑linked immunosorbent assay (ELISA). An in vitro chondrocyte model was established by the introduction of TNF‑α and ox‑LDL, cell death was analyzed by trypan blue assay and the mechanisms were explored based on the apoptosis related pathway and autophagy pathway. Significantly increased ox‑LDL level (70.30±17.83 vs. 37.22±19.97, P<0.05) in SF sample and LOX‑1 expression level (0.51±0.10 vs. 0.32±0.04, P<0.05) in cartilage tissue was found in OA patients compared to those corresponding samples from control subjects. Ox‑LDL could facilitate TNF‑α mediated chondrocyte death and this effect could be blocked by LOX‑1 antibody neutralization. Autophagy inhibition by 3‑MA and Atg‑5 siRNA could reverse the cell death effect mediated by TNF‑α and ox‑LDL co‑treatment on chondrocytes. Oxidized low density lipoprotein facilitates tumor necrosis factor‑α mediated chondrocyte death via its interaction with LOX‑1, and autophagy is involved in the mechanisms.
Pengcheng Shen, Yu Zhu, Lifan Zhu, Fengbiao Weng, Xiaolin Li, Yaozeng Xu

1397 related Products with: Oxidized low density lipoprotein facilitates tumor necrosis factor‑α mediated chondrocyte death via autophagy pathway.

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#29039510   2017/10/10 To Up

Homocysteine‑induced oxidative stress through TLR4/NF‑κB/DNMT1‑mediated LOX‑1 DNA methylation in endothelial cells.

Atherosclerosis (AS) is a progressive disease of multifactorial origin, which occurs in response to endothelial injury. Increased homocysteine (Hcy) is considered a major cause of endothelial dysfunction, oxidative stress and DNA methylation; however, the mechanisms remain to be fully elucidated. The aim of the present study was to investigate whether Hcy causes injury to endothelial cells (ECs) by the effect of lectin‑like oxidized‑low density lipoprotein receptor‑1 (LOX‑1) DNA methylation through toll‑like receptor 4(TLR4)/nuclear factor (NF)‑κB/DNA methyltransferase (DNMT)1. The ECs were treated with different concentrations of Hcy, and it was found that Hcy promoted the expression of TLR4, leading to EC injury. The effect of oxidative stress was analyzed by measuring superoxide dismutase, malondialdehyde and hydrogen peroxide in the ECs. In addition, the association between NF‑κB and DNMT1 was examined by treatment of the ECs with pyrrolidine dithiocarbamate (PDTC). The results suggested that Hcy induced LOX‑1 DNA hypomethyaltion to promote the expression levels of LOX‑1. Taken together, Hcy injured the ECs through the effect of methylation and trans‑sulfuration metabolism of LOX‑1 through TLR4/NF‑κB/DNMT1. Following injury to the ECs, lipids, particularly ox‑LDL, accumulated in the sub‑endothelial layer to promote the formation of AS.
Sheng-Chao Ma, Yin-Ju Hao, Yun Jiao, Yan-Hua Wang, Ling-Bo Xu, Cai-Yan Mao, Xiao-Ling Yang, An-Ning Yang, Jue Tian, Ming-Hao Zhang, Shao-Ju Jin, Hua Xu, Yi-Deng Jiang, Hui-Ping Zhang

2443 related Products with: Homocysteine‑induced oxidative stress through TLR4/NF‑κB/DNMT1‑mediated LOX‑1 DNA methylation in endothelial cells.

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#28983628   2017/09/26 To Up

Long intergenic noncoding RNA p21 mediates oxidized LDL‑induced apoptosis and expression of LOX‑1 in human coronary artery endothelial cells.

Atherosclerosis is the most common pathological cause of cardiovascular diseases, and endothelial dysfunction has a vital role. It has been suggested that inhibiting endothelial cell apoptosis induced by oxidized low‑density lipoprotein (ox‑LDL), an essential atherosclerotic factor, is a potential novel therapeutic strategy against atherosclerosis. Previous studies have revealed that endothelial lectin‑like ox‑LDL receptor‑1 (LOX‑1) and long intergenic noncoding RNA p21 (lincRNA‑p21) may serve as therapeutic targets for atherosclerosis and associated cardiovascular disorders. The present study investigated the role of lincRNA‑p21 in oxLDL‑induced apoptosis and expression of LOX‑1 in human coronary artery endothelial cells (HCAECs). Primary HCAECs were treated with ox‑LDL (30, 60 or 90 µg/ml) for 24 or 48 h, and the expression of lincRNA‑p21, LOX‑1 and cell apoptosis rate were measured. Ox‑LDL dose‑ and time‑dependently induced the expression of lincRNA‑p21 and LOX‑1 and apoptosis in HCAECs. Lentiviral overexpression of lincRNA‑p21 markedly increased oxLDL‑induced apoptosis and the expression of LOX‑1 in HCAECs. Additionally, the effect was largely blocked by selective protein kinase C (PKC) inhibitor, rottlerin. However, lentiviral knockdown of lincRNA‑p21 markedly decreased oxLDL‑induced apoptosis and the expression of LOX‑1. In addition, overexpression and knockdown of lincRNA‑p21 markedly increased and decreased oxLDL‑induced PKCδ activity/phosphorylation, respectively. In conclusion, to the best of our knowledge, the present study provides the first evidence indicating that lincRNA‑p21 is a major mediator of oxLDL‑induced apoptosis and expression of LOX‑1 in human vascular endothelial cells, and acts via activation of PKCδ. These results provide insights into the role of lincRNA‑p21 in the pathogenesis of atherosclerosis.
Tao Zhou, Xiaofang Chen

2003 related Products with: Long intergenic noncoding RNA p21 mediates oxidized LDL‑induced apoptosis and expression of LOX‑1 in human coronary artery endothelial cells.

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#28535009   2017/05/18 To Up

MicroRNA let-7g alleviates atherosclerosis via the targeting of LOX-1 in vitro and in vivo.

Atherosclerosis is a chronic arterial disease and the leading cause of stroke and myocardial infarction. Micro-RNAs (miRNAs or miRs) have been reported to act as essential modulators during the progression of atherosclerosis. Although miR-let-7g has been demonstrated to contribute to maintaining endothelial function and vascular homeostasis, it is not known whether miR-let-7g exerts a therapeutic effect on experimental atherosclerosis. The aim of this study was to investigate the effects of miR-let-7g on atherosclerosis in vivo and in vitro and to explore its underlying mechanisms. Data from our study showed that exogenous lectin‑like oxidized low‑density lipoprotein receptor‑1 (LOX-1 or OLR1) overexpression resulted in the significant promotion of proliferation and migration of human aortic smooth muscle cells (ASMCs), whereas such changes induced by LOX-1 were obviously suppressed by transfection of miR‑let‑7g. We later confirmed that LOX-1 is a potential target of miR-let-7g, and miR-let-7g markedly inhibited LOX-1 expression in ASMCs by directly binding to the 3' untranslated region of LOX-1. Furthermore, in a hyperlipidemic apolipoprotein E knockout (ApoE-/-) mouse model, intravenous delivery of miR-let-7g mimics obviously attenuated high-fat diet-induced neointima formation and atherosclerotic lesions, accompanied by the significant downregulation of LOX-1, which was consistent with the effect of miR-let-7g on ASMCs. Taken together, our data revealed that miR-let-7g exhibits anti-atherosclerotic activity, at least partially by targeting the LOX-1 signaling pathway. This study suggests that miR-let-7g may be a therapeutic candidate for treating atherosclerosis, and provides novel insight into miRNA-based therapy for this disease.
Mingxin Liu, Guizhou Tao, Qifeng Liu, Kun Liu, Xinchun Yang

2432 related Products with: MicroRNA let-7g alleviates atherosclerosis via the targeting of LOX-1 in vitro and in vivo.

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