Toll-like Receptor 8 Stability Is Regulated by Ring Finger 216 in Response to Circulating MicroRNAs

Evankovich, John; Baldwin, Courtney; Chen, Yanwen; White, Virginia A.; Villandre, J.; Londino, J.D.; Liu, Yuan; McVerry, Bryan J.; Kitsios, Georgios D; Mallampalli, Rama K.; Chen, Bill B.

doi:10.1165/rcmb.2018-0373oc

Cited by 13 publications

(10 citation statements)

References 68 publications

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“…Antimirs targeted at miR-122 have reached phase II trials for the treatment of hepatitis. miRNAs, such as miR-146, miR-21, and miR-17, also play an important role in ARDS-associated inflammation ( 17 – 20 ). Sun and colleagues observed that overexpression of miR-181b inhibited the expression of importin-a3 and further reduced lung injury and mortality in ARDS mice ( 21 ).…”

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confidence: 99%

MicroRNA-574-5p Attenuates Acute Respiratory Distress Syndrome by Targeting HMGB1

Zhou

Rui

et al. 2021

Am J Respir Cell Mol Biol

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Acute respiratory distress syndrome (ARDS) is a critical condition with high mortality. HMGB1 (high-mobility group protein B1) is one of the key proinflammatory factors in the ARDS “inflammatory storm.” According to previous studies, some microRNAs (miRNAs) play important roles in this process. We aimed to determine the contributing miRNAs targeting the expression and release of HMGB1. miRNA expression in the peripheral blood of patients with ARDS was measured by miRNA microarray. miRNAs targeting HMGB1 were screened and explored for further study. In LPS-induced cell and mouse ARDS models, we explored the effect of this miRNA on the expression and secretion of HMGB1 by Western blot, real-time qPCR, and ELISA. The effects of this miRNA on the NF-κB signaling pathway, proinflammatory cytokines, and NLRP3 (nod-like receptor protein 3) inflammasome were detected by Western blot and real-time qPCR. In ARDS models, microRNA-574-5p (miR-574-5p) expression could be induced by the TLR4/NF-κB pathway upon LPS stimulation. It could suppress the inflammatory response by targeting HMGB1. Enforcing the expression of miR-574-5p or HMGB1 siRNA silencing inhibits the activation of NF-κB signaling pathway and the NLRP3 inflammasome. Moreover, overexpression of HMGB1 reversed the antiinflammatory effect of miR-574-5p. In ARDS mice, overexpression of miR-574-5p suppresses alveolar leukocytes infiltration, interstitial edema, protein effusion, and inflammation. This study demonstrated that miR-574-5p provided negative feedback to LPS-induced inflammation and relieved ARDS. It may provide new therapeutic strategies for ARDS.

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confidence: 99%

MicroRNA-574-5p Attenuates Acute Respiratory Distress Syndrome by Targeting HMGB1

Zhou

Rui

et al. 2021

Am J Respir Cell Mol Biol

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“…Interestingly, we found that miR-223-3p expression was decreased among nonsurvivors in our cohort. Increased expression of miR-223-3p has previously been reported in the leukocytes and plasma of ARDS patients compared to healthy controls [11] and critically-ill non-ARDS patients [12], suggesting that baseline levels of miR-223 in the absence of ARDS remain low, but expression is increased in ARDS. However, miR-223-3p has been suggested to be protective in murine models of ARDS [13] and associated with decreased expression of IL-6 and IL-1β in macrophages, possibly via targeting STAT3 [14].…”

Section: To the Editormentioning

confidence: 84%

A novel miRNA biomarker panel associated with mortality in pediatric patients with ARDS

2021

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“…Additionally, the ceRNA subnetwork found that downregulated miR-623 and its upregulated HCK and CXCR4 target genes were coregulated by circ_0006725 and circ_0079284. Ring Finger 216 (RNF216) is the host of has_circRNA_0079284, and study reported that it may be involved in innate immune signaling [ 55 ]. Study on intervertebral disc degeneration has shown that miR-623 directly bound CXCL12 to reduce levels of inflammatory factors in LPS-injured nucleus pulposus cells [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics Analysis of Competing Endogenous RNA Network and Immune Infiltration in Atrial Fibrillation

et al. 2022

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Background. There is still no clear understanding of the pathogenesis of atrial fibrillation (AF). For this purpose, we used integrated analysis to uncover immune infiltration characteristics and investigated their relationship with competing endogenous RNA (ceRNA) network in AF. Methods. Three AF mRNA data sets (GSE14975, GSE79768, and GSE41177) were integrated using the SVA method from Gene Expression Omnibus (GEO). Together with AF circRNA data set (GSE129409) and miRNA data set (GSE70887) from GEO database, we built a ceRNA network. Then hub genes were screened by the Cytoscape plug-in cytoHubba from a protein-protein interaction (PPI) network. As well, CIBERSORT was employed to investigate immune infiltration, followed by Pearson correlation coefficients to unravel the correlation between AF-related infiltrating immune cells and hub genes. Ulteriorly, circRNA-miRNA-mRNA regulatory axises that could be immunologically related to AF were obtained. Results. Ten hub genes were identified from the constructing PPI network. The immune infiltration analysis revealed that the number of monocytes and neutrophils was higher, as well as the number of dendritic cells activated and T cells regulatory (Tregs) was lower in AF. Seven hub genes (C5AR1, CXCR4, HCK, LAPTM5, MPEG1, TLR8, and TNFSF13B) were associated with those 4 immune cells ( P < 0.05 ). We found that the circ_0005299–miR-1246–C5AR1 and circRNA_0079284-miR-623-HCK/CXCR4 regulatory axises may be associated with the immune mechanism of AF. Conclusion. The findings of our study provide insights into immuno-related ceRNA networks as potential molecular regulators of AF progression.

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Toll-like Receptor 8 Stability Is Regulated by Ring Finger 216 in Response to Circulating MicroRNAs

Cited by 13 publications

References 68 publications

MicroRNA-574-5p Attenuates Acute Respiratory Distress Syndrome by Targeting HMGB1

MicroRNA-574-5p Attenuates Acute Respiratory Distress Syndrome by Targeting HMGB1

A novel miRNA biomarker panel associated with mortality in pediatric patients with ARDS

Bioinformatics Analysis of Competing Endogenous RNA Network and Immune Infiltration in Atrial Fibrillation

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