MicroRNA-490-3p inhibits inflammatory responses in LPS-induced acute lung injury of neonatal rats by suppressing the IRAK1/TRAF6 pathway

Yang, Guang; Zhao, Yuan

doi:10.3892/etm.2020.9584

Cited by 7 publications

(5 citation statements)

References 42 publications

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“… In one-challenge intervention, mice or rats were injected with or inhaled LPS [ 37 , 61 , 62 , 66 , 70 , 72 – 77 , 80 , 85 ], or were intranasally inoculated with S. pneumoniae [ 41 ], or intraperitoneally inoculated with E . coli [ 79 ], or underwent CLP [ 82 ].…”

Section: Supporting Informationmentioning

confidence: 99%

A systematic review and meta-analyses of interleukin-1 receptor associated kinase 3 (IRAK3) action on inflammation in in vivo models for the study of sepsis

et al. 2022

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Background Interleukin-1 receptor associated kinase 3 (IRAK3) is a critical modulator of inflammation and is associated with endotoxin tolerance and sepsis. Although IRAK3 is known as a negative regulator of inflammation, several studies have reported opposing functions, and the temporal actions of IRAK3 on inflammation remain unclear. A systematic review and meta-analyses were performed to investigate IRAK3 expression and its effects on inflammatory markers (TNF-α and IL-6) after one- or two-challenge interventions, which mimic the hyperinflammatory and immunosuppression phases of sepsis, respectively, using human or animal in vivo models. Methods This systematic review and meta-analyses has been registered in the Open Science Framework (OSF) (Registration DOI: 10.17605/OSF.IO/V39UR). A systematic search was performed to identify in vivo studies reporting outcome measures of expression of IRAK3 and inflammatory markers. Meta-analyses were performed where sufficient data was available. Results The search identified 7778 studies for screening. After screening titles, abstracts and full texts, a total of 49 studies were included in the systematic review. The review identified significant increase of IRAK3 mRNA and protein expression at different times in humans compared to rodents following one-challenge, whereas the increases of IL-6 and TNF-α protein expression in humans were similar to rodent in vivo models. Meta-analyses confirmed the inhibitory effect of IRAK3 on TNF-α mRNA and protein expression after two challenges. Conclusions A negative correlation between IRAK3 and TNF-α expression in rodents following two challenges demonstrates the association of IRAK3 in the immunosuppression phase of sepsis. Species differences in underlying biology affect the translatability of immune responses of animal models to human, as shown by the dissimilarity in patterns of IRAK3 mRNA and protein expression between humans and rodents following one challenge that are further influenced by variations in experimental procedures.

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Section: Supporting Informationmentioning

confidence: 99%

A systematic review and meta-analyses of interleukin-1 receptor associated kinase 3 (IRAK3) action on inflammation in in vivo models for the study of sepsis

et al. 2022

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“…Substantial evidence suggests that miRNAs act as significant mediators in immune system development and thus are implicated in certain inflammatory lung diseases, including ALI [ 9 , 11 ]. Underexpression of miR-490-3p occurred in LPS-induced ALI rats, and restoration of miR-490-3p represses LPS-induced lung epithelial cell injury [ 10 ]. Upregulated miR-26a-5p has been found to attenuate LPS-induced inflammatory responses in ALI mice by reducing levels of proinflammatory cytokines and MDA and MPO activity in LPS-induced A549 cells [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs are highly conserved small noncoding RNAs, 21–23 nucleotides in length, and can regulate relevant genes by inhibiting translation or inducing RNA degradation [ 9 ]. miRNAs serve as critical regulators of cell proliferation, apoptosis, and inflammation [ 10 ]. Growing evidence has demonstrated the effects of miRNAs on inflammatory response in sepsis-induced ALI [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

miR-142-5p Encapsulated by Serum-Derived Extracellular Vesicles Protects against Acute Lung Injury in Septic Rats following Remote Ischemic Preconditioning via the PTEN/PI3K/Akt Axis

et al. 2022

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This study intends to investigate the effects of miR-142-5p encapsulated by serum-derived extracellular vesicles (EVs) on septic acute lung injury (ALI) following remote ischemic preconditioning (RIPC) through a PTEN-involved mechanism. ALI was induced in rats by lipopolysaccharide (LPS) injection, 24 h before which RIPC was performed via the left lower limb. Next, the binding affinity between miR-142-5p and PTEN was identified. EVs were isolated from serum and injected into rats. The morphology of lung tissues, pulmonary edema, and inflammatory cell infiltration into lung tissues were then assessed, and TNF-α and IL-6 levels in serum and lung tissues were measured. The results indicated that RIPC could attenuate ALI in sepsis. miR-142-5p expression was increased in serum, lung tissues, and serum-derived EVs of ALI rats following RIPC. miR-142-5p could target PTEN to activate the PI3K/Akt signaling pathway. miR-142-5p shuttled by serum-derived EVs reduced pulmonary edema, neutrophil infiltration, and TNF-α and IL-6 levels, thus alleviating ALI in LPS-induced septic rats upon RIPC. Collectively, serum-derived EVs-loaded miR-142-5p downregulated PTEN and activated PI3K/Akt to inhibit ALI in sepsis following RIPC, thus highlighting potential therapeutic molecular targets against ALI in sepsis.

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“…Recently, miRNAs have been demonstrated to serve a notable role in the development of several types of diseases and have attracted significant attention. Yang and Zhao ( 30 ) revealed that miR-490-3p upregulation suppressed LPS-induced ALI via the IL-1 receptor-associated kinase 1/TNF receptor-associated factor 6 pathway. Furthermore, Li et al ( 31 ) demonstrated that miR-150 expression was downregulated in an LPS-induced ALI cell model, and that miR-150-overexpression inhibited LPS-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

miR‑122‑5p downregulation attenuates lipopolysaccharide‑induced acute lung injury by targeting IL1RN

Zeng

Wang

2021

Exp Ther Med

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MicroRNAs (miRs) and inflammatory cytokines can induce acute lung injury (ALI), which can develop into acute respiratory distress syndrome in severe cases. Previous research has revealed that miR-122-5p participates in the development of ALI, and that its expression is positively associated with ALI. However, the mechanism by which miR-122-5p contributes to ALI remains to be determined. In the current study, TargetScan and dual luciferase reporter gene assays were used to confirm that IL-1 receptor antagonist (IL1RN) was a target of miR-122-5p. Subsequently, by referring to previous literature, a lipopolysaccharide (LPS)-induced ALI cell model was established. A549 cells were transfected with mimic control or miR-122-5p mimics for 24 h, and 10 µg LPS was used to treat the transfected cells for 12 h. The results revealed that miR-122-5p mimics decreased cell viability and promoted apoptosis. Lactate dehydrogenase (LDH) release assays indicated that miR-122-5p mimics increased LDH release. ELISA demonstrated that miR-122-5p mimics promoted TNF-α, IL-1β and IL-6 expression levels. A549 cells were transfected with inhibitor control, miR-122-5p inhibitor, miR-122-5p inhibitor + control-small interfering (si)RNA or miR-122-5p inhibitor + IL1RN-siRNA for 24 h, after which the cells were treated with 10 µg LPS for 12 h. The results revealed that the effects of the miR-122-5p inhibitor were the opposite of those of the miR-122-5p mimic. All the effects of miR-122-5p inhibitor on LPS-treated A549 cells were significantly reversed by IL1RN-siRNA. Overall, the results highlighted miR-122-5p as a potential novel target for the treatment of ALI.

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MicroRNA-490-3p inhibits inflammatory responses in LPS-induced acute lung injury of neonatal rats by suppressing the IRAK1/TRAF6 pathway

Cited by 7 publications

References 42 publications

A systematic review and meta-analyses of interleukin-1 receptor associated kinase 3 (IRAK3) action on inflammation in in vivo models for the study of sepsis

A systematic review and meta-analyses of interleukin-1 receptor associated kinase 3 (IRAK3) action on inflammation in in vivo models for the study of sepsis

miR-142-5p Encapsulated by Serum-Derived Extracellular Vesicles Protects against Acute Lung Injury in Septic Rats following Remote Ischemic Preconditioning via the PTEN/PI3K/Akt Axis

miR‑122‑5p downregulation attenuates lipopolysaccharide‑induced acute lung injury by targeting IL1RN

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