Role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes via TLR4/ROS/NF-κB pathway

Yu, Jiangkun; Lu, Yanyu; Li, Yapeng; Xiao, Lili; Xing, Yu; Li, Yanshen; Wu, Leiming

doi:10.1111/jphp.12415

Cited by 22 publications

(16 citation statements)

References 33 publications

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“…ROS, which are mainly produced by NADPH oxidase, are commonly considered cytotoxic and can even induce cell damage in high levels ( Ray et al, 2012 ). Previous studies also have shown that ROS were implicated in TLR4-mediated immune reactions ( Zhang et al, 2016 ; Pan et al, 2017 ), and elicited a cascade of inflammatory events, such as activation of NF-κB ( Yu et al, 2015 ; Singh et al, 2016 ). In the present study, miR-181a mimics markedly suppressed the intracellular ROS accumulation in LPS-induced macrophages.…”

Section: Discussionmentioning

confidence: 98%

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

et al. 2018

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Acute lung injury (ALI) is a progressive clinical disease with a high mortality rate, and characterized by an excessive uncontrolled inflammatory response. MicroRNAs (miRNAs) play a critical role in various human inflammatory diseases, and have been recognized as important regulators of inflammation. However, the regulatory mechanisms mediated by miRNAs involved in Lipopolysaccharide (LPS)-induced inflammation in ALI remain hazy. In this study, we found that miR-181a expression in the lung tissues of ALI mice and LPS-stimulated RAW 264.7 macrophages is dramatically reduced. We also show that over-expression of miR-181a significantly decreased the production of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, whereas inhibition of miR-181a reversed this decrease. Moreover, miR-181a inhibits NF-κB activation and accumulation of reactive oxygen species (ROS) by targeting TLR4 expression. We further verify that miR-181a suppresses TLR4 expression by binding directly to the 3′-UTR of TLR4. Therefore, we provide the first evidence for the negative regulation of miR-181a in LPS-induced inflammation via the suppression of ROS generation and TLR4-NF-κB pathway.

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Section: Discussionmentioning

confidence: 98%

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

et al. 2018

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“…An early study that explores the role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes has demonstrated that S100A1 treatment significantly enhanced IL-37 protein or mRNA level, which in turn could attenuate ROS and phospho-p65 NF- κ B levels. Thus, the researchers finally considered that S100A1 could regulate the inflammatory response in H9C2 cells via TLR4/ROS/NF- κ B pathway [80–82]. A recent study also further confirmed that IL-37 exerts anti-inflammatory effects via TLR2/4-NF- κ B signaling pathway.…”

Section: Il-37 Exerts Anti-inflammatory Responses In Hcaecsmentioning

confidence: 99%

Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells

Yan

Xie

et al. 2019

Mediators of Inflammation

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Interleukin-37 (IL-37) is unique in the IL-1 family since it broadly suppresses innate immunity and elevates in humans with inflammatory and autoimmune diseases. IL-37 shows definite groups and transcripts for human IL37 gene, but it is still not completely understood the effect and mechanisms of inflammatory response in endothelial cells. It is well accepted that endothelial dysfunction caused by inflammation is a key initiating event in atherosclerotic plaque formation, which leads to the occurrence and development of the cardiovascular adverse events in clinical since the inflammatory responses of endothelial cells could induce and enhance the deposition of extensive lipid and the formation of atherosclerotic plaque in the intima. Thus, it is essential to investigate the role and potential mechanisms in endothelial inflammatory response to prevent the formation and development of many cardiovascular diseases including atherosclerosis. So far, the recent studies have revealed that IL-37 is able to inhibit inflammatory response by suppressing the TLR2-NF-κB-ICAM-1 pathway intracellularly in human coronary artery endothelial cells (HCAECs). Further, the role of IL-37 may be related to the IL-18 pathway extracellularly and involved in the adhesion and transmigration of neutrophils in HCAECs.

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“…Little is known about cardiac functions of PP5. Recently, it was reported that S100 proteins can modulate PP5 functions [11] and S100A1 that amongst others interacts with the cardiac ryanodine receptor and the Ca 2+ ATPase of the sarcoplasmic reticulum (SERCA), plays an important role in the inflammatory response in cardiomyocytes [12,13]. We have previously generated and described transgenic mice with cardiac specific overexpression of PP5 and demonstrated that PP5 serves as a modulator of cardiac function [14].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of protein phosphatase 5 in the mouse heart: Reduced contractility but increased stress tolerance – Two sides of the same coin?

et al. 2019

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The pathophysiological mechanisms of sepsis-induced cardiac dysfunction are largely unknown. The Toll-like receptor 4 (TLR4) is expressed in cardiac myocytes and is involved in bacterial endotoxin-mediated inflammatory disorders. TLR4 signaling leads to activation of the nuclear factor kappa B followed by increased expression of cytokines. Several protein phosphatases including PP2Cβ, PP2A or PP1 are known to act as regulators of this signaling pathway. Here, we examined the role of PP5 for the inflammatory response to the bacterial endotoxin lipopolysaccharide in the heart using a transgenic mouse model with cardiac myocyte directed overexpression of PP5. In these transgenic mice, basal cardiac contractility was reduced, in vivo as well as in vitro , but LPS-induced cardiac dysfunction was less pronounced compared to wild type mice. Quantitative RT-PCR suggested an attenuated NF-κB signaling in the heart and cardiac expression of heat shock protein 25 (HSP25) was increased in PP5 transgenic mice. From our data we assume that PP5 increases stress tolerance of cardiac myocytes by downregulation of NF-κB signaling and upregulation of HSP25 expression.

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Role of S100A1 in hypoxia-induced inflammatory response in cardiomyocytes via TLR4/ROS/NF-κB pathway

Abstract: Our results demonstrate that S100A1 can regulate the inflammatory response and oxidative stress in H9C2 cells via TLR4/ROS/NF-κB pathway. These findings provide an interesting strategy for protecting cardiomyocytes from hypoxia-induced inflammatory response.

Cited by 22 publications

References 33 publications

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

Downregulation of TLR4 by miR-181a Provides Negative Feedback Regulation to Lipopolysaccharide-Induced Inflammation

Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells

Overexpression of protein phosphatase 5 in the mouse heart: Reduced contractility but increased stress tolerance – Two sides of the same coin?

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