MiR-338-5p Promotes Inflammatory Response of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via Targeting<i>SPRY1</i>

Yang, Yan; Wang, Yanfeng; Liang, Qiong; Yao, Lutian; Gu, Shizhong; Bai, Xiwen

doi:10.1002/jcb.25883

Cited by 14 publications

(5 citation statements)

References 28 publications

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“…a study using different activators of Wnt/β-catenin signaling revealed that Wnt/β-catenin signaling is closely related to trophoblast cell differentiation (35). in addition, decreased expression of WnT2 in the villi of patients with unexplained recurrent spontaneous abortion may cause trophoblast cell dysfunction via suppressing Wnt/β-catenin signaling (36). on this basis, the present study further examined the effects of FaM99a on Wnt/β-catenin signaling activity.…”

Section: Discussionmentioning

confidence: 85%

lncRNA FAM99A is downregulated in preeclampsia and exerts a regulatory effect on trophoblast cell invasion, migration and apoptosis

Qiao

et al. 2019

Mol Med Report

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Preeclampsia (Pe) is a complication of pregnancy, and a leading cause of maternal mortality and morbidity worldwide. recently, the dysregulation of long non-coding rnas (lncrnas) has been reported to contribute to the pathogenesis and progression of Pe. This study aimed to examine the alterations in the lncrna family with sequence similarity 99 member a (FaM99a) in Pe and its effects on trophoblasts. The results of reverse transcription-quantitative Pcr indicated that the expression levels of FaM99a were downregulated in placental tissues from women with severe Pe compared with in those from controls. a Transwell invasion assay and wound healing assay revealed that overexpression of FaM99a promoted invasion and migration of HTr-8/SVneo cells; conversely, knockdown of FaM99a suppressed the invasive and migratory abilities of HTr-8/SVneo cells. Flow cytometry demonstrated that FaM99a overexpression induced a decrease in the apoptotic rate of cells, whereas knockdown of FaM99a increased the apoptotic rate of HTr-8/SVneo cells. Western blot analysis revealed that overexpression of FaM99a decreased the protein expression levels of cleaved caspase-3, cleaved caspase-9 and Bax, and increased Bcl-2 protein expression, whereas knockdown of FaM99a had the opposite effects on these protein levels. overexpression of FaM99a also decreased caspase-3 activity in HTr-8/SVneo cells; however, knockdown of FaM99a increased caspase-3 activity. in addition, overexpression of FaM99a enhanced Wnt/β-catenin signaling activity, whereas FaM99a knockdown exerted an inhibitory effect on the Wnt/β-catenin signaling activity in HTr-8/SVneo cells. in conclusion, these results indicated that FaM99a may serve a role in modulating the functions of trophoblasts, partially via targeting Wnt/β-catenin signaling.

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Section: Discussionmentioning

confidence: 85%

lncRNA FAM99A is downregulated in preeclampsia and exerts a regulatory effect on trophoblast cell invasion, migration and apoptosis

Qiao

et al. 2019

Mol Med Report

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“…62 Studies have also found that miR-338-5p is highly expressed in RA. miR-338-5p can promote the proliferation, invasion, and inflammatory response of RA-FLS by directly downregulating the expression of sprouty RTK signaling antagonist 1 ( SPRY1 ), 63 and also promotes the proliferation and migration of RA-FLS by targeting nuclear factor of activated T cells 5 ( NFAT5 ). 64 Although the current findings on the expression of miR-338-5p in RA are contrary, they also illustrate the potential role of miR-338-5p in RA pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics Analysis Identified the Hub Genes, mRNA–miRNA–lncRNA Axis, and Signaling Pathways Involved in Rheumatoid Arthritis Pathogenesis

Yang¹,

Su²,

Xu³

et al. 2022

IJGM

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Objective Rheumatoid arthritis (RA) is a nonspecific, chronic, systemic autoimmune disease characterized by symmetric polyarticular synovitis. Bioinformatics analysis of potential biomarkers, mRNA–miRNA–lncRNA axes, and signaling pathways in the pathogenesis of RA provides potential targets and theoretical basis for further research on RA. Methods The GSE1919 and GSE77298 datasets were downloaded from the Gene Expression Omnibus database ( http://www.ncbi.nlm.nih.gov/geo ). Perl was used to perform data merging, and R was used to perform batch correction. The “limma” package of R was used to screen differentially expressed genes, and the “clusterProfiler” package was used to perform enrichment analysis of the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Search Tool for the Retrieval of Interacting Genes/Proteins was used to construct the protein–protein interaction network, Cytoscape was used for module analysis, and R was used to screen for hub genes. GraphPad Prism was used to plot the receiver operating characteristic curve of the hub genes. Gene set enrichment analysis and competitive endogenous RNA network analysis were performed on hub genes with the greatest diagnostic values. The hub gene with the greatest diagnostic value was verified using immunohistochemical staining. Results We obtained nine hub genes ( ITGB2, VAMP8, HLA-A, PTAFR, SYK, FCER1G, HLA-DPB1, LCP2 , and ACTR2 ) and four mRNA–miRNA–lncRNA axes (ITGB2-hsa-miR-486-3p-SNHG3, ITGB2-hsa-miR-338-5p-XIST, ITGB2-hsa-miR-5581-3p-XIST, and ITGB2-hsa-miR-1226-5p-XIST) related to the pathogenesis of RA. The nine hub genes were highly expressed, and ITGB2 had the highest diagnostic value for RA. We also identified signaling pathways related to the pathogenesis of RA: Fc epsilon Rl and chemokine signaling pathways. The immunohistochemical results showed that ITGB2 expression was significantly upregulated in RA. Conclusion The hub genes, mRNA–miRNA–lncRNA axes, and signaling pathways related to RA pathogenesis identified in this study provide a new research direction for the mechanism, diagnosis, and treatment of RA.

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“…Even though miR-338-5p has been shown to be related to several human diseases, as well as rheumatoid arthritis [ 33 ], human gastric cancer [ 34 ], pulmonary fibrosis [ 35 ], lung cancer [ 36 ], and glioblastoma [ 37 ], the relationship between miR-338-5p and HS has not been described yet. However, we speculate that miR-338-5p stimulates the cell proliferation, invasion, and the production of cytokines IL-1a, IL-6, and COX2 in HS.…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNAs in Hidradenitis Suppurativa

Felice

Montanino

Mallardo

et al. 2022

Genes

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Hidradenitis suppurativa (HS) is a pathology characterized by chronic inflammation and skin lesions. The molecular basis of the inflammatory network remains unclear; however, since microRNAs (miRNAs) are involved in the modulation of inflammation, the composition of a micro-transcriptome RNA library using the blood of HS patients was analysed here. The total miRNA expression profiles of miRNAs from HS patients was assayed by real-time qPCR. Here, compared to healthy controls, miR-24-1-5p, miR-146a-5p, miR26a-5p, miR-206, miR338-3p, and miR-338-5p expression was found significantly different in HS. Knowing the significance of the miRNA mechanism in inflammatory and immune progression, we suggest that miRNA profiles found in HS patients can be significant in understanding the pathogenesis modality and establishing efficient biomarkers for HS early diagnosis. In particular, miR-338-5p was closely related to HS invasiveness and production of cytokines and was atypically overexpressed. miR-338-5p may represent a good promise as a non-invasive clinical biomarker for HS.

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MiR-338-5p Promotes Inflammatory Response of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via TargetingSPRY1

Cited by 14 publications

References 28 publications

lncRNA FAM99A is downregulated in preeclampsia and exerts a regulatory effect on trophoblast cell invasion, migration and apoptosis

lncRNA FAM99A is downregulated in preeclampsia and exerts a regulatory effect on trophoblast cell invasion, migration and apoptosis

Bioinformatics Analysis Identified the Hub Genes, mRNA–miRNA–lncRNA Axis, and Signaling Pathways Involved in Rheumatoid Arthritis Pathogenesis

Circulating microRNAs in Hidradenitis Suppurativa

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