miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5

Yao, Jun; Gao, Ruoyu; Luo, Ming‐Han; Li, Defeng; Guo, Liliangzi; Yu, Zichao; Xiong, Feng; Wei, Cheng; Wu, Ben-Hua; Xu, Zefeng; Zhang, Dingguo; Wang, Jianyao; Wang, Lisheng

doi:10.1042/bsr20192257

Cited by 6 publications

(4 citation statements)

References 31 publications

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“…Moreover, miR-34a may induce increased level of IL-17 and other proinflammatory cytokines via SIRT1 direct targeting and subsequent induction of NF-κB and the downstream pathway ( Karbasforooshan and Karimi, 2018 ). Remarkably, miR-802 increases Th17 immune response by targeting the suppressor of cytokine signaling (SOCS5) in inflammatory bowel disease ( Yao et al, 2020 ). Apart from immune diseases, the relation between miRNAs and Th17 has been demonstrated in other pathologies.…”

Section: Discussionmentioning

confidence: 99%

Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice

et al. 2022

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Diabetic nephropathy (DN) is the main leading cause of chronic kidney disease worldwide. Although remarkable therapeutic advances have been made during the last few years, there still exists a high residual risk of disease progression to end-stage renal failure. To further understand the pathogenesis of tissue injury in this disease, by means of the Next-Generation Sequencing, we have studied the microRNA (miRNA) differential expression pattern in kidneys of Black and Tan Brachyury (BTBR) ob/ob (leptin deficiency mutation) mouse. This experimental model of type 2 diabetes and obesity recapitulates the key histopathological features described in advanced human DN and therefore can provide potential useful translational information. The miRNA-seq analysis, performed in the renal cortex of 22-week-old BTBR ob/ob mice, pointed out a set of 99 miRNAs significantly increased compared to non-diabetic, non-obese control mice of the same age, whereas no miRNAs were significantly decreased. Among them, miR-802, miR-34a, miR-132, miR-101a, and mir-379 were the most upregulated ones in diabetic kidneys. The in silico prediction of potential targets for the 99 miRNAs highlighted inflammatory and immune processes, as the most relevant pathways, emphasizing the importance of inflammation in the pathogenesis of kidney damage associated to diabetes. Other identified top canonical pathways were adipogenesis (related with ectopic fatty accumulation), necroptosis (an inflammatory and regulated form of cell death), and epithelial-to-mesenchymal transition, the latter supporting the importance of tubular cell phenotype changes in the pathogenesis of DN. These findings could facilitate a better understanding of this complex disease and potentially open new avenues for the design of novel therapeutic approaches to DN.

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Section: Discussionmentioning

confidence: 99%

Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice

et al. 2022

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“…MiR-802 is another miRNA that has been studied in cholesteatoma. Previously, its role was confirmed in mediating the pathogenesis of a variety of tumors [108], obesity [109,110], osteoporosis [111], and inflammatory bowel disease [112].…”

Section: Microrna-802mentioning

confidence: 97%

Expression and Regulatory Mechanisms of MicroRNA in Cholesteatoma: A Systematic Review

Dżaman,

Czerwaty,

Reichert

et al. 2023

IJMS

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Cholesteatoma is a temporal bone disease characterized by dysfunctions of keratinocytes. MicroRNAs (miRNAs) are evolutionary conserved noncoding RNAs that regulate mRNA expression. They can be packaged into exosomes and transported to target cells that can be used in the future therapy of cholesteatoma. This study aimed to collect knowledge on the role of miRNAs and exosomal miRNAs in cholesteatoma and was conducted according to the PRISMA guidelines for systematic reviews. Four databases were screened: Pubmed/MEDLINE, Web of Science, Scopus, and the Cochrane Library. The last search was run on the 6th of June 2023. We included full-text original studies written in English, which examined miRNAs in cholesteatoma. The risk of bias was assessed using the Office of Health Assessment and Translation (OHAT) Risk of Bias Rating Tool, modified for the needs of this review. We identified 118 records and included 18 articles. Analyses revealed the downregulation of exosomal miR-17 as well as miR-10a-5p, miR-125b, miR-142-5p, miR34a, miR-203a, and miR-152-5p and the overexpression of exosomal miR-106b-5p as well as miR-1297, miR-26a-5p, miR-199a, miR-508-3p, miR-21-3p, miR-584-5p, and miR-16-1-3p in cholesteatoma. The role of differentially expressed miRNAs in cholesteatoma, including cell proliferation, apoptosis, the cell cycle, differentiation, bone resorption, and the remodeling process, was confirmed, making them a potential therapeutic target in this disease.

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“…Suppressor of cytokine signaling (SOCS) family members are well‐known negative regulators of cytokine‐dependent signaling. A previous study reported that miR‐802 upregulation aggravated inflammatory bowel disease by suppressing SOCS5 in a mouse model 9 . As a cytokine signaling regulator, SOCS5 is involved in the regulation of inflammatory responses and oxidative stress in chronic obstructive pulmonary disease (COPD) 10 .…”

Section: Introductionmentioning

confidence: 99%

“…A previous study reported that miR-802 upregulation aggravated inflammatory bowel disease by suppressing SOCS5 in a mouse model. 9 As a cytokine signaling regulator, SOCS5 is involved in the regulation of inflammatory responses and oxidative stress in chronic obstructive pulmonary disease (COPD). 10 It also plays a critical role to control several immune diseases such as allergic conjunctivitis.…”

mentioning

confidence: 99%

LncRNA small nucleolar RNA host gene 16 reduces sepsis‐induced myocardial damage by regulating miR‐421/suppressor of cytokine signaling 5 axis

Xie

et al. 2022

The Kaohsiung J of Med Scie

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Currently, sepsis‐induced cardiomyopathy (SIC) remains as one of the most critical clinical syndromes in terminally ill patients. Noncoding RNAs (including microRNAs and long noncoding RNAs) are implicated in both the onset and development of SIC. We herein investigated the functional role and molecular target of long noncoding RNA small nucleolar RNA host gene 16 (SNHG16) in an in vitro SIC model of H9c2 myocardial cells. We used lipopolysaccharide (LPS) as endotoxin to treat H9c2 cells to mimic SIC damages. Cell Counting Kit 8 and apoptosis assay were performed to assess cell proliferation and cell death. Quantitative real‐time‐PCR and Western blot were employed to examine gene expression level at mRNA and protein level. Dual luciferase assay is used to validate the functional interactions between SNHG16/mi‐R421 and miR‐421/suppressor of cytokine signaling 5 (SOCS5). Inflammatory cytokines were measured by ELISA. Superoxide dismutase and malondialdehyde measurement was performed to assess oxidative stress, which was further confirmed by 2′,7′‐dichlorofluorescin diacetate staining. Our data demonstrated that in the LPS‐induced sepsis model of myocardial cells, SNHG16 overexpression downregulated the expression level of miR‐421, which sustained the expression of SOCS5 to alleviate the adverse effects of LPS, such as apoptosis, pro‐inflammatory cytokines, and oxidative stress. Our data suggest that SNHG16 functions as a ceRNA to maintain SOCS5 level by targeting miR‐421, thereby attenuating LPS‐induced myocardial cell damages. Targeting miR‐421 or modulating lncRNA SNHG16 level may be leveraged as a beneficial strategy against sepsis‐induced cellular damage in cardiomyocytes.

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miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5

Cited by 6 publications

References 31 publications

Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice

Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice

Expression and Regulatory Mechanisms of MicroRNA in Cholesteatoma: A Systematic Review

LncRNA small nucleolar RNA host gene 16 reduces sepsis‐induced myocardial damage by regulating miR‐421/suppressor of cytokine signaling 5 axis

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