MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

Qu, Shengming; Yang, Lei; Liu, Zhe

doi:10.1002/jcb.28941

Cited by 25 publications

(15 citation statements)

References 44 publications

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“…Mast cells are important antigen-presenting cells that can release histamine and cytokines through degranulation and act a significant role in the occurrence and development of various inflammatory diseases ( Grabauskas et al, 2020 ; Novruzov, 2008 ; Sajay-Asbaghi et al, 2020 ). Very recently, THBS1 was demonstrated to promote the inflammatory response of mast cells in chronic idiopathic urticaria and the permeability of human dermal microvascular endothelial cells by regulating the TGF-β/SMAD pathway, the effects of which can be inhibited by miR-194 ( Qu, Yang & Liu, 2020 ). Several studies have shown that CXCR4 can promote mast cell chemotaxis to inflammatory sites ( Limón-Flores et al, 2009 ; Lv et al, 2019 ; Patadia et al, 2010 ), and IFRD1 may involve in neutrophilic inflammation in cystic fibrosis ( Blanchard et al, 2011 ; Gu et al, 2009 ; Hector et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

Significance of hub genes and immune cell infiltration identified by bioinformatics analysis in pelvic organ prolapse

Zhao¹,

Xia²,

Lin³

et al. 2020

PeerJ

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Objective Pelvic organ prolapse (POP) refers to the decline of pelvic organ position and dysfunction caused by weak pelvic floor support. The aim of the present study was to screen the hub genes and immune cell infiltration related to POP disease. Methods Microarray data of 34 POP tissues in the GSE12852 gene expression dataset were used as research objects. Weighted gene co-expression network analysis (WGCNA) was performed to elucidate the hub module and hub genes related to POP occurrence. Gene function annotation was performed using the DAVID tool. Differential analysis based on the GSE12852 dataset was carried out to explore the expression of the selected hub genes in POP and non-POP tissues, and RT-qPCR was used to validate the results. The differential immune cell infiltration between POP and non-POP tissues was investigated using the CIBERSORT algorithm. Results WGCNA revealed the module that possessed the highest correlation with POP occurrence. Functional annotation indicated that the genes in this module were mainly involved in immunity. ZNF331, THBS1, IFRD1, FLJ20533, CXCR4, GEM, SOD2, and SAT were identified as the hub genes. Differential analysis and RT-qPCR demonstrated that the selected hub genes were overexpressed in POP tissues as compared with non-POP tissues. The CIBERSORT algorithm was employed to evaluate the infiltration of 22 immune cell types in POP tissues and non-POP tissues. We found greater infiltration of activated mast cells and neutrophils in POP tissues than non-POP tissues, while the infiltration of resting mast cells was lower in POP tissues. Moreover, we investigated the relationship between the type of immune cell infiltration and hub genes by Pearson correlation analysis. The results indicate that activated mast cells and neutrophils had a positive correlation with the hub genes, while resting mast cells had a negative correlation with the hub genes. Conclusions Our research identified eight hub genes and the infiltration of three types of immune cells related to POP occurrence. These hub genes may participate in the pathogenesis of POP through the immune system, giving them a certain diagnostic and therapeutic value.

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Section: Discussionmentioning

confidence: 99%

Significance of hub genes and immune cell infiltration identified by bioinformatics analysis in pelvic organ prolapse

Zhao¹,

Xia²,

Lin³

et al. 2020

PeerJ

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“…As one of the miRNAs, miR-194 was known to promote prostate cancer metastasis by inhibiting SOCS2 to activate STAT3 and ERK signaling pathways [11]. Moreover, miR-194 has been identified to relieve inflammatory response through inhibition of the TGF-β/SMAD signaling pathway activation in chronic idiopathic urticarial [12]. Besides, in renal ischemia-reperfusion injury, upregulation of miR-194 can restrain the secretion of proinflammatory cytokines such as IL-1β, IL-6 and TNF-α [13].…”

Section: Introductionmentioning

confidence: 99%

Suppressed nuclear factor-kappa B alleviates lipopolysaccharide-induced acute lung injury through downregulation of CXCR4 mediated by microRNA-194

et al. 2020

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Acute lung injury (ALI) is a highly lethal pulmonary disease that causes edema, hypoxemia and respiratory failure. Recent evidence indicates that nuclear factor-kappa B (NF-κB) plays a crucial role in ALI development. However, the regulatory mechanism of NF-κB on ALI remains enigmatic. In this study, we investigated potential molecular mechanism of NF-κB on ALI induced by lipopolysaccharide (LPS). BALB/c mice were subjected to intratracheal spraying of LPS to generate an ALI mode, with the activity of NF-κB in mice tissues being detected by enzyme linked immunosorbent assay (ELISA), and the number of inflammatory cells in bronchoalveolar lavage fluid being counted. Then, the macrophage cell line RAW264.7 exposed to LPS were treated with ammonium pyrrolidinedithiocarbamate (PDTC) (inhibitor of NF-κB), miR-194 mimic, or oe-chemokine receptor type 4 (CXCR4) separately or in combination. After that, ELISA and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were used to detect the expression level of IL-1β, IL-6, TNF-α, miR-194 and CXCR4, respectively. In addition, the targeting relationship between miR-194 and CXCR4 was verified by dual-luciferase reporter gene assay. The dry/ wet ratio of lung and the MPO activity were also measured to assess the inflammatory response in mice. Activation of NF-κB down-regulated the miR-194 expression in LPS-induced ALI. Overexpression of miR-194 alleviated LPSinduced ALI and reduced the expression of inflammatory factors IL-1β, IL-6 and TNF-α via targeting CXCR4. In LPSinduced ALI, NF-κB mediates the CXCR4 expression by inhibiting the expression of miR-194, thus promoting the inflammatory injury of lung.

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“…33 There is overwhelming evidence that miRNAs are regulators of the inflammatory response, [34][35][36][37] some of which are associated with inflammatory diseases such as osteoarthritis (OA) and RA. 38 Qu et al 39…”

Section: Biological Functionsmentioning

confidence: 99%

“…There is overwhelming evidence that miRNAs are regulators of the inflammatory response, 34‐37 some of which are associated with inflammatory diseases such as osteoarthritis (OA) and RA 38 . Qu et al 39 found that miR‐194 inhibits the activation of the TGF‐β/SMAD pathway, thereby mitigating inflammation in chronic idiopathic urticaria. Xia et al 40 reported that miR‑217 and miR‑543 are associated with the SIRT1/AMPK/NF‑κB pathway, and downregulation of these two miRNAs alleviates the inflammatory response in children with viral myocarditis.…”

Section: Mirnamentioning

confidence: 99%

Functional interaction between long non‐coding RNA and microRNA in rheumatoid arthritis

Liu

Wen

et al. 2020

Clinical Laboratory Analysis

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MicroRNA (miRNA) has received widespread attention for its role in several key cellular processes such as cell differentiation, cell proliferation, apoptosis, and autoimmune diseases. Although we now have a good understanding of miRNA expression and function, our knowledge regarding the molecular mechanism of long non‐coding RNA (lncRNA) is still in its infancy. In this review, we will briefly introduce the definition and function of lncRNA and summarize the interactions between lncRNA and miRNA and their research progress in rheumatoid arthritis (RA). The expression of miR‐16, miR‐146a, miR‐155, and miR‐223 and the interactions between HOTAIR and miR138, ZFAS1 and miR‐27a, and GAPLINC and miR‐575 are representative examples that may augment the understanding of the pathogenesis of RA and help in the development of new biomarkers and target therapies.

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MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

Cited by 25 publications

References 44 publications

Significance of hub genes and immune cell infiltration identified by bioinformatics analysis in pelvic organ prolapse

Significance of hub genes and immune cell infiltration identified by bioinformatics analysis in pelvic organ prolapse

Suppressed nuclear factor-kappa B alleviates lipopolysaccharide-induced acute lung injury through downregulation of CXCR4 mediated by microRNA-194

Functional interaction between long non‐coding RNA and microRNA in rheumatoid arthritis

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