The roles of <scp>SOCS</scp>3 and <scp>STAT</scp>3 in bacterial infection and inflammatory diseases

Gao, Yu; Zhao, Honglei; Wang, Peng; Wang, Jun; Zou, Lili

doi:10.1111/sji.12727

Cited by 98 publications

(73 citation statements)

References 141 publications

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“…STAT3 has been implicated in a variety of physiological and pathophysiological processes, including inflammatory responses, cell proliferation and differentiation, cell adhesion, tissue regeneration, and angiogenesis [43]. For example, STAT3 affects pro-inflammatory and anti-inflammatory responses under the stimulation of IL-6, IL-10, and other cytokines [44]. In addition, in the acute phase of viral infection, most viruses inhibit STAT3 to reduce the ability of host cells to respond to inflammatory cytokines in the body, while eliminating negative feedback from the antiviral response of the body, suggesting that STAT3 is a potential target for antiviral therapy [43].…”

Section: Discussionmentioning

confidence: 99%

Network analysis of the pharmacological mechanism of Reduning injection in the treatment of novel coronavirus pneumonia

Xie

Zheng

Jiang³

et al. 2020

Preprint

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Background: Pneumonia caused by novel coronavirus (COVID-19) is spreading worldwide. Traditional Chinese medicines (TCM) have played an important role in COVID-19 treatment in China. This study explores the specific mechanisms of action of Reduning injection (RDN) as a novel clinical treatment for COVID-19. Material and Methods: We collected RDN chemical components and targets, COVID-19-related targets, and predictions of potential targets of RDN treatment for COVID-19 and performed network topology, Gene Ontology (GO) functional enrichment analysis and WikiPathways enrichment analysis of these potential targets. Results: This study identified 14 chemical components and 200 targets of RDN; 3,558 COVID-19-related targets; 54 potential targets of RDN treatment for COVID-19. GO functional enrichment analysis identified 83 entries in biological process, including regulation of vasoconstriction、arachidonic acid secretion, and 17 entries in molecular function, including oxidoreductase activity, acting on the aldehyde or oxo group of donors. WikiPathways enrichment analysis identified 16 entries including the interleukin-12 signaling pathway. Conclusion: In brief, RDN may be involved in the core anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) action and also in the reduction of the resulting inflammatory response, oxidative stress, and lung tissue damage, and the regulation of apoptosis, providing evidence for the characteristics of TCM in COVID-19 treatment involving multiple components, targets, and pathways.

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Section: Discussionmentioning

confidence: 99%

Network analysis of the pharmacological mechanism of Reduning injection in the treatment of novel coronavirus pneumonia

Xie

Zheng

Jiang³

et al. 2020

Preprint

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“…For example, down-regulation of PVT1 correlates with the differentiation of Th17 cells and the duration of multiple sclerosis, a chronic immune-mediated disease (Eftekharian et al, 2017). Additionally, PVT1 promotes the production of inflammatory cytokines to aggravate the progression of IL-1β-stimulated osteoarthritis (Zhao et al, 2018). Overexpressed PVT1 can enhance the expression of IL-6 and IL-1β in a nonbinding manner by regulating the nuclear factor-κB (NF-κB) pathway, which is considered a critical mechanism in the regulation of immune and inflammatory processes, and ultimately aggravating septic acute kidney injury (Huang et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Peer Review #2 of "Comprehensive analysis of an lncRNA-miRNA-mRNA competing endogenous RNA network in pulpitis (v0.1)"

2019

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Background. Pulpitis is a common inflammatory disease that affects dental pulp. It is important to understand the molecular signals of inflammation and repair associated with this process. Increasing evidence has revealed that long noncoding RNAs (lncRNAs), via competitively sponging microRNAs (miRNAs), can act as competing endogenous RNAs (ceRNAs) to regulate inflammation and reparative responses. The aim of this study was to elucidate the potential roles of lncRNA, miRNA and messenger RNA (mRNA) ceRNA networks in pulpitis tissues compared to normal control tissues. Methods. The oligo and limma packages were used to identify differentially expressed lncRNAs and mRNAs (DElncRNAs and DEmRNAs, respectively) based on expression profiles in two datasets, GSE92681 and GSE77459 , from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were further analyzed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Protein-protein interaction (PPI) networks and modules were established to screen hub genes using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the Molecular Complex Detection (MCODE) plugin for Cytoscape, respectively. Furthermore, an lncRNA-miRNA-mRNA-hub genes regulatory network was constructed to investigate mechanisms related to the progression and prognosis of pulpitis. Then, quantitative real-time polymerase chain reaction (qRT-PCR) was applied to verify critical lncRNAs that may significantly affect the pathogenesis in inflamed and normal human dental pulp. Results. A total of 644 upregulated and 264 downregulated differentially expressed genes (DEGs) in pulpitis samples were identified from the GSE77459 dataset, while 8 up-and 19 downregulated probes associated with lncRNA were identified from the GSE92681 dataset. Protein-protein interaction (PPI) based on STRING analysis revealed a network of DEGs containing 4,929 edges and 623 nodes. Upon combined analysis of the constructed PPI network and the MCODE results, 10 hub genes, including IL6, IL8, PTPRC, IL1B, TLR2, ITGAM, CCL2, PIK3CG, ICAM1, and PIK3CD, were detected in the network. Next, a ceRNA regulatory relationship consisting of one lncRNA (PVT1), one miRNA (hsa-miR-455-5p) and two mRNAs (SOCS3 and PLXNC1) was established. Then, we constructed the network in which the regulatory relationship between ceRNA and hub genes was summarized. Finally, our qRT-PCR results confirmed significantly higher levels of PVT1 transcript in inflamed pulp than in normal pulp tissues (p=0.03). Conclusion. Our study identified a novel lncRNA-mediated ceRNA regulatory mechanisms in the pathogenesis of pulpitis.

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“…In the cytoplasm of an “inflamed” cell, the physiologic SOCS 1 and 3 control the availability of transcription factors known as STAT 1 and 3 . These transactivators regulate the genes encoding multiple cytokines and chemokines including IFNγ, IL‐2, IL‐4, IL‐6, IL‐7, IL‐15, IL‐17, the leukaemia inhibitory factor, leptin and the granulocyte‐colony stimulating factor (G‐CSF) . The cytoplasmic tails of their receptors as well as the signal transducers, JAK, are targeted by SOCS1 and SOCS3 for ubiquitin‐mediated proteasomal degradation while simultaneously being destroyed by the same mechanism .…”

Section: Intracellular Protein Therapy With Cell‐penetrating Recombinmentioning

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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The roles of SOCS3 and STAT3 in bacterial infection and inflammatory diseases

Cited by 98 publications

References 141 publications

Network analysis of the pharmacological mechanism of Reduning injection in the treatment of novel coronavirus pneumonia

Network analysis of the pharmacological mechanism of Reduning injection in the treatment of novel coronavirus pneumonia

Peer Review #2 of "Comprehensive analysis of an lncRNA-miRNA-mRNA competing endogenous RNA network in pulpitis (v0.1)"

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

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