A novel pleiotropic effect of aspirin: Beneficial regulation of pro- and anti-inflammatory mechanisms in microglial cells

Kata, D; Földesi, Imre; Feher, L; Hackler, László; Puskás, László G.; Gulya, Károly

doi:10.1016/j.brainresbull.2017.05.009

Cited by 30 publications

(25 citation statements)

References 83 publications

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“…The expression levels were shown in Additional file 11 : Figure S5. The results indicated that some of the potentially targeted genes, like C4BPA [ 35 ], MASP1 [ 36 ], MBL2 [ 37 ], ORM1 [ 38 ], APOA2 [ 39 ], KNG1 [ 40 ], are significantly downregulated upon knocking down the lncRNAs (Fig. 5a and Additional file 12 : Figure S6a),.On the contrary, the expression of these genes except for ORM1 appeared significantly increased when we overexpressed APOC1P1 in CCA cell line (Additional file 12 : Figure S6b and c), suggesting that the inflammatory genes could be regulated by the selected lncRNAs in CCA cells.…”

Section: Resultsmentioning

confidence: 99%

Global identification and characterization of lncRNAs that control inflammation in malignant cholangiocytes

Han

Wei

et al. 2018

BMC Genomics

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BackgroundLong noncoding RNAs (lncRNAs) are known to play important roles in different cell contexts, including cancers. However, little is known about lncRNAs in cholangiocarcinoma (CCA), a cholangiocyte malignancy with poor prognosis, and associated with chronic inflammation and damage to the biliary epithelium. This study determined whether lncRNAs were dysregulated and participated in disease diagnosis or pivotal inflammation pathways through a genome-wide lncRNA screening and functional analysis.ResultsWe firstly identified a large number of lncRNAs abnormally expressed between 9 pairs of cancerous and adjacent tissues of CCA, and between intra-hepatic CCA and extra-hepatic CCA through a genome-wide profiling. A set of aberrant differentially expressed lncRNAs were further validated in a training set (16 pairs) and a test set (11 pairs) of CCA patient samples. Following assessment of the diagnostic value of the 7 differentially expressed lncRNAs, we confirmed the optimal combination of H19, C3P1, AC005550.3, PVT1, and LPAL2 with area under the curve of 0.8828 [95% CI: 0.7441–1.021, P < 0.001], with 93.75% sensitivity and 81.25% specificity, at the cutoff point of − 0.2884 to distinguish the CCA tissue from the normal ones, suggesting that specific lncRNAs may have potential for detecting CCA. More importantly, the genome-wide locus and lncRNA/mRNA co-expression analyses revealed a set of lncRNAs that participated in inflammation and oxidative stress response pathways by regulating genes in cis or in trans. Finally, APOC1P1, PVT1, and LPAL2 were validated to regulate the migration and some pivotal inflammation genes under the CCA pathogenesis.ConclusionsOur findings are the first to show that lncRNAs may not only be potential biomarkers of CCA progression but also respond to inflammation in CCA.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-5133-8) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Global identification and characterization of lncRNAs that control inflammation in malignant cholangiocytes

Han

Wei

et al. 2018

BMC Genomics

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“…Studies showed that deletion of Kng1 protein in ischemic mice reduced thrombosis and inflammation (Langhauser et al, 2012 ). Also Kng1 as a pro-inflammatory cytokine, Which promotes the development of cellular inflammation (Langhauser et al, 2012 ; Kata et al, 2017 ). In this study, STRING database revealed that Kng1 is a downstream target gene of Ednrb.…”

Section: Discussionmentioning

confidence: 99%

Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway

et al. 2018

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Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by chronic exposure to cigarette smoke (CS). Celastrol is a pentacyclic triterpenoid compound exhibits potent antioxidant and anti-inflammatory activities. Also it is presently known to protect against liver damage induced by type II diabetes. However, its role in COPD is unclear. In this study, we investigated the effects of Celastrol on cellular inflammation in mice exposed to CS and Beas-2B cells treated with CS extract (CSE). C57BL/6 mice and Beas-2B cells were randomly divided into three groups: control group, COPD or CSE group, and Celastrol treatment group. The COPD mice models were subjected to smoke exposure and cell models were treated with CSE. Bioinformatics analysis was performed to identify differentially expressed genes following treatment with Celastrol in COPD, the molecular networks was mapped by Cytoscape. The levels of inflammatory cytokinesinterleukin-8, tumor necrosis factor α, monocyte chemoattractant protein-1, and oxidative stress factors superoxide dismutase and catalase were measured by enzyme-linked immunosorbent assay. Hematoxylin and eosin staining to detect the injury of mouse lung tissue. mRNA and protein levels of Ednrb and Kng1 in the tissues and cells were measured by quantitative polymerase chain reaction (PCR) and western blotting, respectively. Apoptosis was measured by flow cytometry and TUNEL staining. Compared to mice in the COPD group, mice treated with Celastrol had significantly reduced levels of inflammatory cytokines interleukin-8, tumor necrosis factor α and monocyte chemoattractant protein-1 in the serum and bronchoalveolar lavage fluid, and significantly increased levels of oxidative stress factors superoxide dismutase and catalase. The same results were obtained at the cellular level using Beas-2B cells. Compared to the model groups, Celastrol reduced lung injury in mice and significantly reduced cellular apoptosis. Bioinformatics analysis showed that Ednrb is a target gene of Celastrol and differentially expressed in COPD. Quantitative PCR analysis showed that Ednrb expression in patients with COPD was significantly increased compared to that in healthy controls. Additionally, Celastrol effectively reduced Ednrb/Kng1 expression in both cell and animal models. Celastrol has a therapeutic effect on COPD and may alleviate COPD by inhibiting inflammation development by suppressing the Ednrb/Kng1 signaling pathway.

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“…Rats were allowed to adapt to the environment for one week before the experiments. Animal experimental procedures were performed according to the Guide for Care and Use of Laboratory Animals ( 15 , 16 ) and protocols were approved by the Animal Experiment Ethics Committee of The First People's Hospital (Wuhan, China).…”

Section: Methodsmentioning

confidence: 99%

Sufentanil attenuates inflammation and oxidative stress in sepsis-induced acute lung injury by downregulating KNG1 expression

Wang

Han

et al. 2020

Mol Med Rep

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The present study aimed to investigate the effects of sufentanil on sepsis-induced acute lung injury (ali), and identify the potential molecular mechanisms underlying its effect. in order to achieve this, a rat sepsis model was established. Following treatment with sufentanil, the lung wet/dry (W/d) weight ratio was calculated. Histopathological analysis was performed via hematoxylin and eosin staining. Levels of inflammatory factors in bronchoalveolar lavage fluid were determined via eliSa. Furthermore, malondialdehyde (Mda) content and the activities of superoxide dismutase (Sod), catalase (caT) and glutathione peroxidase (GSH-Px) in tissue homogenates were assessed using commercial kits. Western blot analysis was performed to determine kininogen-1 (KnG1) protein expression. in addition, alveolar epithelial type ii cells (aec ii) were stimulated with lipopolysaccharide (LPS) to mimic ALI. The levels of inflammation and oxidative stress were evaluated following overexpression of KnG1. Protein expression levels of nuclear factor-κB (nF-κB) and nuclear factor erythroid 2-related factor 2 (nrf2)/heme oxygenase-1 (Ho-1) signaling were determined via western blot analysis. The results of the present study demonstrated that sufentanil alleviated histopathological injury and the W/d ratio in lung tissue. Following treatment with sufentanil, levels of inflammatory factors also decreased, accompanied by decreased concentrations of Mda, and increased activities of Sod, caT and GSH-Px. notably, KnG1 was decreased in lung tissues following treatment with sufentanil. Furthermore, overexpression of KnG1 attenuated the inhibitory effects of sufentanil on lPS-induced inflammation and oxidative stress in aec ii. Sufentanil markedly downregulated nF-κB expression, while upregulating nrf2 and Ho-1 expression levels, which was reversed following overexpression of KnG1. Taken together, the results of the present study suggested that sufentanil may alleviate inflammation and oxidative stress in sepsis-induced ali by downregulating KnG1 expression.

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A novel pleiotropic effect of aspirin: Beneficial regulation of pro- and anti-inflammatory mechanisms in microglial cells

Cited by 30 publications

References 83 publications

Global identification and characterization of lncRNAs that control inflammation in malignant cholangiocytes

Global identification and characterization of lncRNAs that control inflammation in malignant cholangiocytes

Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway

Sufentanil attenuates inflammation and oxidative stress in sepsis-induced acute lung injury by downregulating KNG1 expression

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