Anti-Inflammatory Activity of Adenosine 5′-Trisphosphate in Lipopolysaccharide-Stimulated Human Umbilical Vein Endothelial Cells Through Negative Regulation of Toll-Like Receptor MyD88 Signaling

Luo, Xuan; Xiao, Bo-Lin; Xiao, Zunqi

doi:10.1089/dna.2019.4773

Cited by 3 publications

(3 citation statements)

References 28 publications

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“…The first is the increased expression of IL-1β in macrophages. Stimulation of TLR4 with LPS can lead to activation of the transcription factor NF-κB and then induce the expression of proinflammatory molecules such as IL-1β 38 . The second is that IL-1β overproduction is a consequence of increased macrophages numbers.…”

Section: Discussionmentioning

confidence: 99%

CCR5 signaling promotes lipopolysaccharide-induced macrophage recruitment and alveolar developmental arrest

et al. 2021

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The pathogenesis of bronchopulmonary dysplasia (BPD), involves inflammatory, mechanisms that are not fully characterized. Here we report that overexpression of C-C chemokine receptor 5 (CCR5) and its ligands is associated with BPD development. Lipopolysaccharide-induced BPD rats have increased CCR5 and interleukin-1β (IL-1β) levels, and decreased alveolarization, while CCR5 or IL-1β receptor antagonist treatments decreased inflammation and increased alveolarization. CCR5 enhances macrophage migration, macrophage infiltration in the lungs, IL-1β levels, lysyl oxidase activity, and alveolar development arrest. CCR5 expression on monocytes, and its ligands in blood samples from BPD infants, are elevated. Furthermore, batyl alcohol supplementation reduced CCR5 expression and IL-1β production in lipopolysaccharide-exposed rat lungs. Moreover, receptor-interacting kinase 3 (RIP3) upstream regulator of CCR5-cultured RIP3−/− macrophages exhibited partly blocked lipopolysaccharide-induced CCR5 expression. We conclude that increased CCR5 expression is a key mechanism in BPD development and represents a novel therapeutic target for treatment.

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Section: Discussionmentioning

confidence: 99%

CCR5 signaling promotes lipopolysaccharide-induced macrophage recruitment and alveolar developmental arrest

et al. 2021

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“…To verify these findings, further in-depth studies are required. For example, the expression levels of CD14 and TLR4, which may influence the extent of the LPS response (42), should be measured following miR-144-5p overexpression. In addition, the role of miR-144-5p and TLR2 in an in vivo model of RA and the correlation of miR-144-5p expression with the clinicopathological characteristics of patients with RA will also need to be studied in the future.…”

Section: Discussionmentioning

confidence: 99%

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

Zhou

et al. 2019

Exp Ther Med

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The aim of the present study was to explore the possible role of microRNA-144-5p (miR-144-5p) in rheumatoid arthritis (RA) and the associated mechanism. Following the induction of THP-1 cell differentiation into macrophages by phorbol ester (100 ng/ml) treatment, an in vitro inflammatory model of RA was established by treating the THP-1 macrophages with 1 µg/ml lipopolysaccharide (LPS). The level of miR-144-5p was subsequently measured using reverse transcription-quantitative PCR, which found that the expression of miR-144-5p was significantly reduced in LPS-treated THP-1 macrophages. Bioinformatics analysis and a dual-luciferase reporter assay were used to predict and confirm TLR2 as a direct target of miR-144-5p, respectively. Toll-like receptor 2 (TLR2) was then validated as a target gene of miR-144-5p. The effects of miR-144-5p upregulation and TLR2 silencing on LPS-treated THP-1 macrophages were then determined by transfection with miR-144-5p mimic and TLR2-siRNA, respectively. Cell viability was subsequently measured using a Cell Counting Kit-8 assay, whilst the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8 secreted by THP-1 macrophages was measured using ELISA. Western blotting was performed to measure p65 phosphorylation (p-p65) in the NK-κB signaling pathway. It was found that miR-144-5p overexpression reduced macrophage cell viability, reduced the expression of TNF-α, IL-6 and IL-8, and reduced the expression of TLR2 and p-p65 compared with the control group. Likewise, TLR2 silencing also reduced macrophage cell viability and reduced the expression of TNF-α, IL-6 and IL-8 in THP-1 macrophages. In conclusion, the data from the present study suggested that miR-144-5p overexpression reduced THP-1 macrophage cell viability and inhibited the expression of TNF-α, IL-6 and IL-8 in cells, possibly by inhibiting the expression of TLR2 and suppressing the activation of NK-κB signaling. Therefore, miR-144-5p may serve as a novel therapeutic target for the treatment of RA.

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“…Previous studies have shown that adenosine or its analogues could raise intraocular angiogenic factors and inflammatory cytokines, such as vascular endothelial growth factor, insulin-like growth factor-1, basic fibroblast growth factor, interleukin-8, and angiogenin-2 ( Feoktistov et al, 2003 ; Haskó and Pacher, 2012 ). Luo et al (2019 ) found that adenosine attenuated the inflammatory response of human endothelial cells through negative regulation of Toll-like receptor MyD88 signal. Haas et al (2011 ) showed that adenosine could induce a reduction of Toll-like receptor4 expression at the surface of human macrophages, resulting in a robust inhibition of TNF-α production.…”

Section: Discussionmentioning

confidence: 99%

Metabolite Changes in the Aqueous Humor of Patients With Retinal Vein Occlusion Macular Edema: A Metabolomics Analysis

Xiong

Chen

et al. 2021

Front. Cell Dev. Biol.

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Macular edema (ME) is the main cause of visual impairment in patients with retinal vein occlusion (RVO). The degree of ME affects the prognosis of RVO patients, while it lacks objective laboratory biomarkers. We aimed to compare aqueous humor samples from 28 patients with retinal vein occlusion macular edema (RVO-ME) to 27 age- and sex-matched controls by ultra-high-performance liquid chromatography equipped with quadrupole time-of-flight mass spectrometry, so as to identify the key biomarkers and to increase the understanding of the mechanism of RVO-ME at the molecular level. Through univariate and multivariate statistical analyses, we identified 60 metabolites between RVO-ME patients and controls and 40 differential metabolites in mild RVO-ME [300 μm ≤ central retinal thickness (CRT) < 400 μm] patients compared with severe RVO-ME (CRT ≥ 400 μm). Pathway enrichment analysis showed that valine, leucine, and isoleucine biosynthesis; ascorbate and aldarate metabolism; and pantothenate and coenzyme A biosynthesis were significantly altered in RVO-ME in comparison with controls. Compared with mild RVO-ME, degradation and biosynthesis of valine, leucine, and isoleucine; histidine metabolism; beta-alanine metabolism; and pantothenate and coenzyme A biosynthesis were significantly changed in severe RVO-ME. Furthermore, the receiver operating characteristic (ROC) curve analysis revealed that adenosine, threonic acid, pyruvic acid, and pyro-L-glutaminyl-l-glutamine could differentiate RVO-ME from controls with an area under the curve (AUC) of >0.813. Urocanic acid, diethanolamine, 8-butanoylneosolaniol, niacinamide, paraldehyde, phytosphingosine, 4-aminobutyraldehyde, dihydrolipoate, and 1-(beta-D-ribofuranosyl)-1,4-dihydronicotinamide had an AUC of >0.848 for distinguishing mild RVO-ME from severe RVO-ME. Our study expanded the understanding of metabolomic changes in RVO-ME, which could help us to have a good understanding of the pathogenesis of RVO-ME.

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Anti-Inflammatory Activity of Adenosine 5′-Trisphosphate in Lipopolysaccharide-Stimulated Human Umbilical Vein Endothelial Cells Through Negative Regulation of Toll-Like Receptor MyD88 Signaling

Cited by 3 publications

References 28 publications

CCR5 signaling promotes lipopolysaccharide-induced macrophage recruitment and alveolar developmental arrest

CCR5 signaling promotes lipopolysaccharide-induced macrophage recruitment and alveolar developmental arrest

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

Metabolite Changes in the Aqueous Humor of Patients With Retinal Vein Occlusion Macular Edema: A Metabolomics Analysis

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