The essential role of p38 MAPK in mediating the interplay of oxLDL and IL-10 in regulating endothelial cell apoptosis

Yin, Yanlin; Liu, Weiwei; Ji, Guo; Dai, Yue

doi:10.1016/j.ejcb.2013.01.001

Cited by 36 publications

(25 citation statements)

References 55 publications

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“…The binding of ligands to LOX-1 induces the activation of p38 mitogen-activated protein kinase (p38MAPK), phosphatidylinositol-3-kinase, and extracellular signal-regulated kinase (ERK1/2), which leads to activation of transcription factor nuclear factor-kB (Li et al, 2000;Tanigawa et al, 2006). These signal pathways promote the production of proinflammatory cytokines (such as tumor necrosis factor-a, interleukin-6,10) and elicit expression of adhesion molecules such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 (Li et al, 2002;Hashizume and Mihara, 2012;Yin et al, 2013). These mediators lead to macrophage/monocyte attachment and activation, further inducing the expression of LOX-1.…”

Section: Discussionmentioning

confidence: 99%

Serum sLOX-1 Levels Are Correlated with the Presence and Severity of Obstructive Sleep Apnea

Li²,

Wu³

et al. 2015

Genetic Testing and Molecular Biomarkers

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Context: Inflammation plays a critical role in the development and progression of obstructive sleep apnea (OSA). Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) activation is involved in the pathophysiology of inflammatory process-related disorders. Objective: This study aims to investigate whether serum soluble LOX-1 (sLOX-1) levels are associated with the presence and severity of OSA. Materials and Methods: A total of 137 OSA patients and 78 controls were recruited in this study. Serum sLOX-1 levels were measured by enzyme-linked immunosorbent assay. The severity of OSA was assessed by the apnea-hypopnea index (AHI). Results: OSA patients had significantly higher serum sLOX-1 levels compared with controls. Serum sLOX-1 levels elevated with the increment of OSA severity. sLOX-1 was the independent predictor of OSA. Serum sLOX-1 levels were significantly correlated with AHI and high-sensitivity C-reactive protein levels. Conclusions: Serum sLOX-1 levels were independently correlated with the presence and severity of OSA. These findings revealed that sLOX-1 might function as a potential biomarker for monitoring the development and progression of OSA.

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Section: Discussionmentioning

confidence: 99%

Serum sLOX-1 Levels Are Correlated with the Presence and Severity of Obstructive Sleep Apnea

Li²,

Wu³

et al. 2015

Genetic Testing and Molecular Biomarkers

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“…Despite its lower expression, p38β can potentially perform overlapping roles with p38α, whereas p38γ and p38δ have more restricted expression patterns [45]. Recently, many studies have reported that the inhibition of p38 MAPK phosphorylation could either lead to or explain the beneficial effects of particular compound and proteins on cell apoptosis [46,47,48]. In the present investigation, we focussed on the relationship between RSV and p38 MAPK in the ox-LDL-mediated apoptosis of RAW264.7 macrophages.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Suppresses Oxidised Low-Density Lipoprotein-Induced Macrophage Apoptosis through Inhibition of Intracellular Reactive Oxygen Species Generation, LOX-1, and the p38 MAPK Pathway

Guo

Liu

et al. 2014

Cell Physiol Biochem

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Background/Aim: Resveratrol (RSV) may have therapeutic potential for various diseases. Here we investigated the effect of RSV on oxidised low-density lipoprotein- (ox-LDL) induced apoptosis in RAW264.7 macrophages. Methods: Apoptosis of macrophages following incubation with ox-LDL (with or without RSV pre-treatment) was detected by flow cytometry. Western blotting was used to assess the protein expression of Bax, Bcl-2, and caspase-3 as well as ox-LDL receptor 1 (LOX-1) and p38 mitogen-activated protein kinase (MAPK) phosphorylation. Reactive oxygen species (ROS) generation was evaluated by 2', 7'-dichlorofluorescein diacetate, and JC-1 probe was used to determine the mitochondrial transmembrane potential of cells. Results: Ox-LDL significantly reduced viability and increased the rate of apoptosis (P < 0.05) in RAW264.7 cells. However, pre-treatment with RSV resulted in a remarkable decrease in this apoptotic effect. Moreover, ox-LDL caused the up-regulation of Bax and the down-regulation of Bcl-2, as well as the activation of caspase-3. Expression of LOX-1, phosphorylation of p38 MAPK, and intracellular ROS production also increased after ox-LDL stimulation. Strikingly, these effects were abolished by pre-treatment of cells with RSV. Conclusion: RSV suppresses ox-LDL-induced macrophage apoptosis. These beneficial effects might be exerted through inhibition of ROS generation, LOX-1, and the p38 MAPK signalling pathway.

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“…P38 activation is thought to be involved in the apoptosis of endothelial cells (61,62). The P38 inhibitor, SB203580, partly decreased the endothelial cell apoptosis, in our studies, and is a key event in the pathogenesis of arthrosclerosis.…”

Section: Discussionmentioning

confidence: 59%

Irradiated U937 Cells Trigger Inflammatory Bystander Responses in Human Umbilical Vein Endothelial Cells through the p38 Pathway

Xiao

Liu

et al. 2014

Radiation Research

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Radiation-induced bystander effects are a well-known phenomenon that are observed when treating cancer and other diseases after radiotherapy, and even after occupational exposure to radiation. However, little is known about the crosstalk between irradiated macrophages and endothelial cells that line the circulatory system, which may play a role in the development of atherosclerosis. In the current study, we found that the expression of inducible nitric oxide synthase (iNOS) and the intracellular level of nitric oxide (NO) in gamma-irradiated U937 macrophage cells were significantly increased. When human umbilical vein endothelial cells (HUVECs) were co-cultured with gamma-irradiated U937 cells, additional micronuclei (MN) and apoptosis were induced so that the plating efficiency of the bystander HUVECs decreased and P38 was overexpressed in the bystander HUVECs cells. In addition, the contents of vascular cell adhesion molecule 1 (VCAM-1) and the activities of matrix metalloproteinase-9 (MMP-9) in the culture medium of bystander HUVECs were increased. Furthermore, during cell co-culture the adhesive ability of irradiated U937 cells to the bystander HUVECs increased. When U937 cells were treated with 500 μM S-methylisothiourea sulfate (SMT) (iNOS inhibitor) before irradiation, and HUVECs were treated with 10 μM SB203580 (p38 inhibitor) before cell co-culture or treated with 20 μM c-PTIO (NO scavenger) in the co-culture medium, the bystander micronuclei and the amounts of VCAM-1 and MMP-9 in the medium of bystander HUVECs were diminished, and the ability of irradiated U937 cells adhering to HUVECs was also reduced, while the plating efficiency of bystander HUVECs partially recovered. These results demonstrated that irradiated U937 cells appear to release nitric oxide and thereby further trigger apoptosis and inflammatory responses in the bystander HUVECs through a p38-dependent pathway.

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The essential role of p38 MAPK in mediating the interplay of oxLDL and IL-10 in regulating endothelial cell apoptosis

Cited by 36 publications

References 55 publications

Serum sLOX-1 Levels Are Correlated with the Presence and Severity of Obstructive Sleep Apnea

Serum sLOX-1 Levels Are Correlated with the Presence and Severity of Obstructive Sleep Apnea

Resveratrol Suppresses Oxidised Low-Density Lipoprotein-Induced Macrophage Apoptosis through Inhibition of Intracellular Reactive Oxygen Species Generation, LOX-1, and the p38 MAPK Pathway

Irradiated U937 Cells Trigger Inflammatory Bystander Responses in Human Umbilical Vein Endothelial Cells through the p38 Pathway

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