Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1.

Open Life Sci

Department of Burn and Plastic Surgery, Linyi People's Hospital, No. 27, Jiefang Rd, Linyi City, 276000, Shandong Province, China.

Published: July 2020

Circulating miR-150-5p has been identified as a prognostic marker in patients with critical illness and sepsis. Herein, we aimed to further explore the role and underlying mechanism of miR-150-5p in sepsis. Quantitative real-time-PCR assay was performed to detect the expression of miR-150-5p upon stimulation with lipopolysaccharide (LPS) in RAW264.7 cells. The levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured by ELISA assay. Cell apoptosis was determined using flow cytometry. Western blot was used to assess notch receptor 1 (Notch1) expression in LPS-induced RAW264.7 cells. Dual-luciferase reporter assay was employed to validate the target of miR-150-5p. Our data showed that miR-150-5p was downregulated and Notch1 was upregulated in LPS-stimulated RAW264.7 cells. miR-150-5p overexpression or Notch1 silencing alleviated LPS-induced inflammatory response and apoptosis in RAW264.7 cells. Moreover, Notch1 was a direct target of miR-150-5p. Notch1 abated miR-150-5p-mediated anti-inflammation and anti-apoptosis in LPS-induced RAW264.7 cells. miR-150-5p alleviated LPS-induced inflammatory response and apoptosis at least partly by targeting Notch1 in RAW264.7 cells, highlighting miR-150-5p as a target in the development of anti-inflammation and anti-apoptosis drugs for sepsis treatment.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874594PMC
http://dx.doi.org/10.1515/biol-2020-0058DOI Listing

Publication Analysis

Top Keywords

raw2647 cells
24
lps-induced inflammatory
12
inflammatory response
12
response apoptosis
12
mir-150-5p
9
apoptosis raw2647
8
targeting notch1
8
lps-induced raw2647
8
target mir-150-5p
8
cells mir-150-5p
8

Similar Publications

Jinyinqingre Oral Liquid alleviates LPS-induced acute lung injury by inhibiting the NF-κB/NLRP3/GSDMD pathway.

Chin J Nat Med

June 2023

School of Pharmaceutical Sciences, Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, China. Electronic address:

Acute lung injury (ALI) is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers, resulting in high incidence and mortality rates. Currently, there is a lack of safe and effective drugs for the treatment of ALI. In a previous clinical study, we observed that Jinyinqingre oral liquid (JYQR), a Traditional Chinese Medicine formulation prepared by the Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, exhibited notable efficacy in treating inflammation-related hepatitis and cholecystitis in clinical settings.

View Article and Find Full Text PDF

Fasting protects liver from ischemic injury through Sirt1-mediated downregulation of circulating HMGB1 in mice.

J Hepatol

August 2014

Swiss Hepato-Pancreatico-Biliary Center, Department of Surgery, University Hospital Zürich, CH-8091 Zürich, Switzerland. Electronic address:

Background & Aims: Fasting and calorie restriction are associated with a prolonged life span and an increased resistance to stress. The protective effects of fasting have been exploited for the mitigation of ischemic organ injury, yet the underlying mechanisms remain incompletely understood. Here, we investigated whether fasting protects liver against ischemia reperfusion (IR) through energy-preserving or anti-inflammatory mechanisms.

View Article and Find Full Text PDF

Objective: To investigate the effect of RNA interfering TLR4 signal pathway on phagocytosis of Kupffer cells.

Methods: RAW2647 mice mononuclear macrophage leukemia cells were observed. The tested group was interfered by Tlr4-mus-1567 RNA which had the best result confirmed by QPCR, cells interfered by Negative Control RNA as NC group, and normal cell as control.

View Article and Find Full Text PDF

Coordinate regulation of TLR-mediated arachidonic acid mobilization in macrophages by group IVA and group V phospholipase A2s.

J Immunol

March 2009

Instituto de Biología y Genética Molecular, Consejo Superior de Investigaciones Científicas, and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Valladolid, Spain.

Macrophages can be activated through TLRs for a variety of innate immune responses. In contrast with the wealth of data existing on TLR-dependent gene expression and resultant cytokine production, very little is known on the mechanisms governing TLR-mediated arachidonic acid (AA) mobilization and subsequent eicosanoid production. We have previously reported the involvement of both cytosolic group IVA phospholipase A(2) (cPLA(2)) and secreted group V phospholipase A(2) (sPLA(2)-V) in regulating the AA mobilization response of macrophages exposed to bacterial LPS, a TLR4 agonist.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!