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

Deng, Xiaoyan; Lin, Zhixing; Zuo, Chao; Fu, Yanjie

doi:10.1515/biol-2020-0058

Cited by 13 publications

(10 citation statements)

References 30 publications

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“…Decrease in the expression of miR-150-5p, miR-375, miR-122-5p, and miR-494-3p in COVID-19 patients is a sign of inflammation and an impaired immunity [ 10 , 26–31 ] ( Fig. 4 ).…”

Section: Resultsmentioning

confidence: 99%

Cellular miR-150-5p may have a crucial role to play in the biology of SARS-CoV-2 infection by regulating nsp10 gene

2021

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The role for circulating miRNAs as biomarkers of the COVID-19 disease remains uncertain. We analysed the circulating miRNA profile in twelve COVID-19 patients with moderate-severe disease. This analysis was conducted by performing next generation sequencing (NGS) followed by real-time polymerase chain reaction (RT-qPCR). Compared with healthy controls, we detected significant changes in the circulating miRNA profile of COVID-19 patients. The miRNAs that were significantly altered in all the COVID-19 patients were miR-150-5p, miR-375, miR-122-5p, miR-494-3p, miR-3197, miR-4690-5p, miR-1915-3p, and miR-3652. Infection assays performed using miRNA mimics in HEK-293 T cells determined miR-150-5p to have a crucial role in SARS-CoV-2 infection and this was based on the following data: (i) miR-150-5p mimic lowered in vitro SARS-CoV-2 infection; (ii) miR-150-5p inhibitor reversed the effects of miR-150-5p mimic on SARS-CoV-2 infection of cells; and (iii) a novel miRNA recognition element (MRE) was identified in the coding strand of SARS-CoV-2 nsp10 , the expression of which could be inhibited by miR-150-5p mimic. Our findings identified crucial miRNA footprints in COVID-19 patients with moderate-severe disease. A combination of co-transfection and Western blotting experiments also determined the ability of miR-150-5p to inhibit SARS-CoV-2 infection via directly interacting with MRE in the coding strand of nsp10 . Our investigation showed that a sharp decline in the miR-150-5p plasma levels in COVID-19 patients may support enhanced SARS-CoV-2 infection. Furthermore, this study provides insight into one possible mechanism by which COVID-19-induced changes to miR-150-5p levels may promote SARS-CoV-2 infection via modulating nsp10 expression.

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“…Decrease in the expression of miR-150-5p, miR-375, miR-122-5p, and miR-494-3p in COVID-19 patients is a sign of inflammation and an impaired immunity [ 10 , 26–31 ] ( Fig. 4 ).…”

Section: Resultsmentioning

confidence: 99%

Cellular miR-150-5p may have a crucial role to play in the biology of SARS-CoV-2 infection by regulating nsp10 gene

2021

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“…miR-150 targets notch receptor 1, STAT1 and NF-kB to inhibit LPS-induced apoptosis and IL-1b, IL-6 and TNF, ICAM-1, VCAM-1 and E-selectin in RAW 264.7 macrophages, THP-1 monocytic cells and endothelial cells (150,154,155). miR-150-5p is decreased in the heart of rats challenged with LPS.…”

Section: Anti-inflammatory Activitymentioning

confidence: 99%

Modes of action and diagnostic value of miRNAs in sepsis

et al. 2022

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Sepsis is a clinical syndrome defined as a dysregulated host response to infection resulting in life-threatening organ dysfunction. Sepsis is a major public health concern associated with one in five deaths worldwide. Sepsis is characterized by unbalanced inflammation and profound and sustained immunosuppression, increasing patient susceptibility to secondary infections and mortality. microRNAs (miRNAs) play a central role in the control of many biological processes, and deregulation of their expression has been linked to the development of oncological, cardiovascular, neurodegenerative and metabolic diseases. In this review, we discuss the role of miRNAs in sepsis pathophysiology. Overall, miRNAs are seen as promising biomarkers, and it has been proposed to develop miRNA-based therapies for sepsis. Yet, the picture is not so straightforward because of the versatile and dynamic features of miRNAs. Clearly, more research is needed to clarify the expression and role of miRNAs in sepsis, and to promote the use of miRNAs for sepsis management.

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“…As a secretory protein, CCN plays a major role in many biological processes. [26][27][28][29] In addition, CCN3 has the ability to recruit macrophages and promote their M2 phenotypic differentiation. [29] CCN3 may inhibit the activity of NOTCH1 by binding to the extracellular domain of NOTCH1, [30] which is consistent with the anti-in ammatory effect of CCN3/NOTCH1 signaling pathway on macrophage polarization.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide pretreated bone marrow mesenchymal stem cells derived exosomes promote M2 macrophage polarization through CCN3/NOTCH1 pathway

Yu¹,

Liu²,

Zhou³

2022

Preprint

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Background and Objectives: Exosomes secreted by bone marrow mesenchymal stem cells (BMSCs) pretreated with lipopolysaccharide (LPS) (L-Exo) exert a stronger anti-inflammatory effect than exosomes derived from BMSCs (Exo); exosomes are likely to exert biological effects through carrier proteins. This study aimed to investigate whether L-Exo reduces the inflammatory response after sepsis by overexpressing a specific protein. Methods:The effects of L-Exo and Exo in the treatment of sepsis models in vitro (LPS stimulating Raw264.7) were compared, and their differential proteins were analyzed by mass spectrometry. The mechanism of anti-inflammatory effect of proteins carried by exosomes was evaluated by Western blot, qRT-PCR, ELISA, cell transfection, and TUNEL. Results:ELISA showed that the concentration of TNF-a in the supernatant of septic model treated with L-Exo (131.60 mg/mL) was lower than that in the Exo group (170.85 mg/mL). WB and qRT-PCR showed that the expression of TNF-a and iNOS protein was lowest in the L-Exo group, but no obvious apoptotic cells were detected in TUNEL staining. A total of 154 proteins with significant differences were obtained; CCN3 is one of the upregulated differential proteins. In this study, we verified L-Exo’s anti-inflammatory effect by downregulating NOTCH1 signal to promote M2 polarization via cell transfection and qRT-PCR. Conclusion: L-Exo exerts an anti-inflammatory effect by promoting macrophages polarization to M2 through CCN3/NOTCH1 pathway but is not related to macrophage apoptosis pathway.

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

Cited by 13 publications

References 30 publications

Cellular miR-150-5p may have a crucial role to play in the biology of SARS-CoV-2 infection by regulating nsp10 gene

Cellular miR-150-5p may have a crucial role to play in the biology of SARS-CoV-2 infection by regulating nsp10 gene

Modes of action and diagnostic value of miRNAs in sepsis

Lipopolysaccharide pretreated bone marrow mesenchymal stem cells derived exosomes promote M2 macrophage polarization through CCN3/NOTCH1 pathway

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