Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice

Wang, Wenlong; Zhu, Yitang; Yin, Linlin; Deng, Yaoyao; Chu, Guoxian; Liu, Supin

doi:10.1007/s10753-020-01279-w

Cited by 9 publications

(6 citation statements)

References 19 publications

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“…28 Additionally, inhibition of miR-497 suppresses the expression of inflammatory cytokines and C-reactive protein in hepatic tissues of SpT4-infected mice, including IL-6 and TNF-α. 29 In this study, we found that knockdown of TIMP2 did not affect the expression of MED1, but restored the inhibitory effects of MED1 on IκBα and p65, and increased the hepatocyte apoptosis. The above results indicated that MED1 inhibited the NF-κB pathway and suppressed apoptosis by promoting TIMP2 expression.…”

Section: Mir-497-5p Promotes Nf-κb Pathway and Liver Damage By Inhimentioning

confidence: 49%

“…Importantly, overexpression of TIMP‐2 has been reported to inhibit microglial activation through repression of the activity of NF‐κB 28 . Additionally, inhibition of miR‐497 suppresses the expression of inflammatory cytokines and C‐reactive protein in hepatic tissues of SpT4‐infected mice, including IL‐6 and TNF‐α 29 . In this study, we found that knockdown of TIMP2 did not affect the expression of MED1, but restored the inhibitory effects of MED1 on IκBα and p65, and increased the hepatocyte apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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Downregulation of miR‐497‐5p prevents liver ischemia‐reperfusion injury in association with MED1/TIMP‐2 axis and the NF‐κB pathway

Tao

et al. 2021

The FASEB Journal

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Liver ischemia-reperfusion (I/R) injury is a common clinical pathological phenomenon, which is accompanied by the occurrence in liver transplantation. However, the underlying mechanism is not yet fully understood. MicroRNAs (miRNAs) play an important role in liver I/R injury. Therefore, the study of miRNAs function will contribute a new biological marker diagnosis of liver I/R injury. This study aims to evaluate effects of miR-497-5p in liver I/R injury in mice. The related regulatory factors of miR-497-5p in liver I/R injury were predicted by bioinformatics analysis. Vascular occlusion was performed to establish the liver I/R injury animal models. Hypoxia/ reoxygenation (H/R) was performed to establish the in vitro models. Hematoxylineosin (HE) staining was conducted to assess liver injury. The inflammatory factors were evaluated by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was adopted to assess the cell apoptosis. The expression of miR-497b-5p was increased in liver I/R injury. Knockdown of miR-497b-5p inhibited the production of inflammatory factors and cell apoptosis. Overexpression of mediator complex subunit 1 (MED1) and tissue inhibitor of metalloproteinase 2 (TIMP2) inhibited cell apoptosis to alleviate liver I/R injury. miR-497b-5p could activate the nuclear 2 of 12 | WU et al. factor kappa-B (NF-κB) pathway by inhibiting the MED1/ TIMP-2 axis to promote liver I/R injury. This study may provide a new strategy for the treatment of liver I/R injury.

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Section: Mir-497-5p Promotes Nf-κb Pathway and Liver Damage By Inhimentioning

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Downregulation of miR‐497‐5p prevents liver ischemia‐reperfusion injury in association with MED1/TIMP‐2 axis and the NF‐κB pathway

Tao

et al. 2021

The FASEB Journal

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“…35, 36 PCT, a sensitive biomarker, is often used to detect lung inflammation in humans. 37 Results indicated that RA could significantly inhibit TNF-α, IL-1β and PCT expression in the serum of mice with LPS-induced lung injury and increase IL-10 expression, thereby exerting an inhibitory effect on inflammation.…”

Section: Discussionmentioning

confidence: 91%

Rhubarb Anthraquinones Ameliorates Inflammatory Lung Injury by Enhancing Alveolar Epithelium Tight Junction Proteins through RhoA/ROCK1 Signalling

Liu

Bai

Leng

et al. 2023

Pharmacognosy Magazine

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Background: Leakage of the alveolar epithelial barrier can lead to pulmonary oedema, leading to organ dysfunction. Objectives: Combination anthraquinone (CA) and free anthraquinone (FA) were extracted from Rhubarb, and the prevention and therapeutic effects of Rhubarb anthraquinones (RA) on lipopolysaccharide (LPS)-induced lung injury were investigated. Materials and Methods: The CA and FA were extracted from Rhubarb by water solvent extraction and ethanol solvent extraction. The extracted RA content was determined using spectrophotometry and high-performance liquid chromatography (HPLC). A mouse model of inflammatory lung injury was established by LPS induction to study the mechanism of RA activity. Inflammatory factors were measured using an enzyme-linked immunosorbent assay. Changes in alveolar epithelial leakage were assessed using a permeability assay. Changes in lung injury were evaluated by histopathological and ultrastructural observations. Tight junction (TJ) markers and Ras homolog gene family member A (RhoA)/Rho-associated protein kinase 1 (ROCK1) pathway-related proteins were measured using immunohistochemistry and Western blotting. As an agonist of RhoA/Rock signalling, U46619 was used to further verify whether RA acts through this pathway. Results: RA could inhibit pulmonary inflammation by decreasing the level of inflammatory factors. The alveolar epithelial permeability was reduced, and the pathological injury of the lung tissue was alleviated after administration with RA. Furthermore, the expression of TJ proteins was up regulated and RhoA/ROCK1 signalling was inhibited in the presence of RA. The effects of RA on TJ proteins were partially reversed by U46619. Conclusion: RA effectively protects mice against inflammatory lung injury by enhancing alveolar epithelial TJ via RhoA/ROCK1 signalling.

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“…These results suggested that PepO-induced up-regulation of miR-155 was useful for promoting phagocytosis in PEMs and host guard reaction against pneumococcus and staphylococcus aureus. In addition, the expression of procalcitonin in lung tissue,C-reactive protein, inflammatory cytokines (containing interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)) of S. pneumoniae infected mice could be reduced by suppressing of miR-497-3p expression,which would eventually improve bacterial pneumonia in mice [37]. MiR-30a-5p silencing had a protective effect on pulmonary fibrosis in S. pneumoniae infected mice, reduced the inflammatory cell infiltration, and enhanced the biochemical function of lung.…”

Section: Mirna and Pneumococcal Pneumoniamentioning

confidence: 99%

The role and mechanism of microRNAs in infections with Streptococcus pneumoniae

Qin¹,

Pan

Lu³

et al. 2022

Preprint

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Streptococcus pneumoniae (S. pneumoniae) is the most important pathogenic bacteria occurred in wide range of habitat, which cause of several diseases, including pneumonia, meningitis, otitis media, bacteremia and other common infections. Every year, approximately 1.6 million people are seriously affected and ultimately die as a result of pneumococcal infections worldwide, affecting people’s lives and health. Relevant studies in recent years have demonstrated the important role of microRNAs (miRNAs) in a variety of diseases. Further research on the mechanism of microRNA and the relationship between microRNA and diseases has shown that microRNA may become a new biological marker for disease diagnosis and may also provide a new approach to disease treatment. The function of microRNA in pneumococcal infections has also been gradually reported, including pneumococcal nasopharyngeal colonization, pneumonia, sepsis, bacteremia, heart invasion, meningitis, acute otitis media, osteoarthritis and other diseases. This article will overview the mechanism and research progress of microRNA in infections caused by S. pneumoniae.

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Inhibition of miR-497-3p Downregulates the Expression of Procalcitonin and Ameliorates Bacterial Pneumonia in Mice

Cited by 9 publications

References 19 publications

Downregulation of miR‐497‐5p prevents liver ischemia‐reperfusion injury in association with MED1/TIMP‐2 axis and the NF‐κB pathway

Downregulation of miR‐497‐5p prevents liver ischemia‐reperfusion injury in association with MED1/TIMP‐2 axis and the NF‐κB pathway

Rhubarb Anthraquinones Ameliorates Inflammatory Lung Injury by Enhancing Alveolar Epithelium Tight Junction Proteins through RhoA/ROCK1 Signalling

The role and mechanism of microRNAs in infections with Streptococcus pneumoniae

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