Endothelial microRNAs regulating the NF‐κB pathway and cell adhesion molecules during inflammation

Liu, Zhong; Simard, Martin J.; Huot, Jacques

doi:10.1096/fj.201701536r

Cited by 151 publications

(96 citation statements)

References 104 publications

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“…Endothelial lesion leading to thrombosis is accompanied by an increased ICAM expression, a marker of inflammatory stress (Torres and Sanjuliani, ). ICAM participates in the leukocytes adhesion and their migration to the subendothelial layer may occlude partial or entirely the arterial vessel and therefore lead to a thrombotic event (Zhong et al, ).…”

Section: Resultsmentioning

confidence: 99%

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Benincasa

Filho

Carneiro

et al. 2019

Cell Biology International

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Hyperbaric oxygen is a clinical treatment that contributes to wound healing by increasing fibroblasts proliferation, collagen synthesis, and production of growth factors, inducing angiogenesis and inhibiting antimicrobial activity. It also has been shown that hyperbaric oxygen treatment (HBO), through the activation of nitric oxide synthase promotes an increase in the nitric oxide levels that may improve endothelial progenitor cells (EPC) mobilization from bone marrow to the peripheral blood and stimulates the vessel healing process. However, cellular mechanisms involved in cell proliferation and activation of EPC after HBO treatment remain unknown. Therefore, the present work aimed to analyze the effect of HBO on the proliferation of pre-treated bone marrow-derived EPC with TNF-alpha. Also, we investigated the expression of ICAM and eNOS by immunochemistry, the production of reactive species of oxygen and performed an in vitro wound healing. Although 1h of HBO treatment did not alter the rate of in vitro wound closure or cell proliferation, it increased eNOS expression and decreased ICAM expression and reactive oxygen species production in cells pre-treated with TNF-alpha. These results indicate that HBO can decrease the inflammatory response in endothelial cells mediated by TNF-alpha, and thus, promote vascular recovery after injury.Additional supporting information may be found online in the Supporting Information section at the end of the article. Figure S1. Effect of 100% oxygen on ICAM expression.HBO affects activated EPC proliferation J. C. Benincasa et al.

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Section: Resultsmentioning

confidence: 99%

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Benincasa

Filho

Carneiro

et al. 2019

Cell Biology International

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“…We further investigated the process and its related mechanisms for ROS production and its subsequent oxidative damage triggered by an overload of intracellular calcium ions. ERK MAPK, a ubiquitous signal transduction regulator in mammalian cells (44), together with NF-kB, a member of the transcription factor family and a target of MAPK (45), responds to extracellular stimuli and contributes to xenobiotic-induced oxidative damage (1,46). The uniqueness of the response to various stimuli through this pathway may reside in the extent of the phosphorylation and activation of other cofactors, such as the IKK family, a family of kinases that plays an important role in the activation of IkB, resulting in the release of NF-kB for nuclear translocation and activation of gene transcription (47).…”

Section: Discussionmentioning

confidence: 99%

Fenvalerate induces oxidative hepatic lesions through an overload of intracellular calcium triggered by the ERK/IKK/NF‐κB pathway

et al. 2018

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Fenvalerate (FEN), a mainstream pyrethroid pesticide, was initially recommended as a low‐toxicity agent for controlling agricultural and domestic pests. Despite the widespread use of FEN worldwide, little data are available on FEN‐induced hepatic lesions and molecular mechanisms. In the present study, we first performed an occupational cross‐sectional study on FEN factory workers and found that the levels of serum alanine aminotransferase (ALT) and total antioxidant capacity increased, whereas malondialdehyde decreased in laborers in the working areas where the levels of airborne FEN were much higher compared with the office area. The results were then confirmed by animal experiments that abnormal hepatic histology, increased ALT level, and compromised hepatic oxidative capability were observed in rats exposed to a high concentration of FEN. Furthermore, the bioinformatics analysis of gene microarray in rat liver tissue showed that FEN significantly changed the expressions of genes related to the regulation of intracellular calcium ion homeostasis and the calcium signal pathway. Finally, the functional experiments in Buffalo rat liver (BRL) cells demonstrated that FEN first activated ERK MAPK, followed by IKK and NF‐κB, which triggered the transcription of genes responsible for accelerating an overload of intracellular calcium ions, prompted reactive oxygen species generation in the mitochondria, and finally, induced hepatic cellular apoptosis. The calcium signaling pathway and in particular, an overload of intracellular calcium play a critical role in this pathophysiological process via the ERK/IKK/NF‐κB pathway. Our study furthers the understanding of the mechanism of FEN‐induced hepatic injuries and may have implications in the prevention and control of liver diseases induced by environmental pesticides.—Qiu, L.‐L., Wang, C., Yao, S., Li, N., Hu, Y., Yu, Y., Xia, R., Zhu, J., Ji, M., Zhang, Z., Wang, S.‐L. Fenvalerate induces oxidative hepatic lesions through an overload of intracellular calcium triggered by the ERK/IKK/NF‐κB pathway. FASEB J. 33, 2782–2795 (2019). http://www.fasebj.org

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“…Mediators include cytokines, chemokines, haemopoietic/vascular growth factors and cognate receptors. Moreover, intercellular and intracellular inflammatory responses are mediated by cell adhesion molecules, such as vascular cell adhesion molecule‐1, integrin α4, complement proteins and signal transducers, for example COX‐2 . The genes that encode all these mediators are regulated by transcription factors.…”

Section: Detectors and Mediators Of Inflammatory Insultsmentioning

confidence: 99%

“…Moreover, intercellular and intracellular inflammatory responses are mediated by cell adhesion molecules, such as vascular cell adhesion molecule-1, integrin α4, complement proteins and signal transducers, for example COX-2. [26][27][28][29][30][31] The genes that encode all these mediators are regulated by transcription factors. The activation of proinflammatory transcription factors is controlled by physiologic suppressors of cytokine signalling (SOCS) and other intracellular adaptors (eg ubiquitin-modifying dual enzyme termed A20 protein).…”

Section: Of Inflammatory Insultsmentioning

confidence: 99%

Decoding inflammation, its causes, genomic responses, and emerging countermeasures

Hawiger

Zienkiewicz

2019

Scand J Immunol

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Inflammation is the mechanism of diseases caused by microbial, autoimmune, allergic, metabolic and physical insults that produce distinct types of inflammatory responses. This aetiologic view of inflammation informs its classification based on a cause‐dependent mechanism as well as a cause‐directed therapy and prevention. The genomic era ushered in a new understanding of inflammation by highlighting the cell's nucleus as the centre of the inflammatory response. Exogenous or endogenous inflammatory insults evoke genomic responses in immune and non‐immune cells. These genomic responses depend on transcription factors, which switch on and off a myriad of inflammatory genes through their regulatory networks. We discuss the transcriptional paradigm of inflammation based on denying transcription factors’ access to the nucleus. We present two approaches that control proinflammatory signalling to the nucleus. The first approach constitutes a novel intracellular protein therapy with bioengineered physiologic suppressors of cytokine signalling. The second approach entails control of proinflammatory transcriptional cascades by targeting nuclear transport with a cell‐penetrating peptide that inhibits the expression of 23 out of the 26 mediators of inflammation along with the nine genes required for metabolic responses. We compare these emerging anti‐inflammatory countermeasures to current therapies. The transcriptional paradigm of inflammation offers nucleocentric strategies for microbial, autoimmune, metabolic, physical and other types of inflammation afflicting millions of people worldwide.

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Endothelial microRNAs regulating the NF‐κB pathway and cell adhesion molecules during inflammation

Cited by 151 publications

References 104 publications

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

Fenvalerate induces oxidative hepatic lesions through an overload of intracellular calcium triggered by the ERK/IKK/NF‐κB pathway

Decoding inflammation, its causes, genomic responses, and emerging countermeasures

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