MicroRNA‑129 plays a protective role in sepsis‑induced acute lung injury through the suppression of pulmonary inflammation via the modulation of the TAK1/NF‑κB pathway

Yao, Wenjian; Liu, Xu; Jing, Xue; Li, Saisai; Li, Wei

doi:10.3892/ijmm.2021.4972

Cited by 10 publications

(5 citation statements)

References 58 publications

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“…For example, miR‐326 could target TLR4 to mitigate sepsis‐induced ALI 35 . MiR‐129/TAK1 axis plays a protective role in sepsis‐induced ALI by regulating the NF‐κB pathway 36 . Here, we initially confirmed ROCK1 was a downstream molecule of miR‐26a‐5p to mediate sepsis‐induced ALI via influencing cell death and cell pyroptosis.…”

Section: Discussionmentioning

confidence: 62%

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lncRNA NEAT1 mediates LPS‐induced pyroptosis of BEAS‐2B cells via targeting miR‐26a‐5p/ROCK1 axis

Fan

Ma²,

Tang

et al. 2023

The Kaohsiung J of Med Scie

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Acute lung injury (ALI) is an adverse disease of the respiratory system, and one of its prevalent causes is sepsis induction. Cell pyroptosis facilitates the progression of ALI and lncRNAs play critical roles in ALI. Thus, this research seeks to investigate the specific mechanism of NEAT1 in sepsis‐ALI.BEAS‐2B cells were exposed to lipopolysaccharide (LPS) to construct a cell model of sepsis‐induced ALI. The gene and protein expression were assessed using qRT‐PCR and western blot. Cell viability was identified by CCK‐8. Cell death was discovered using PI staining. The secretion of IL‐1β and IL‐18 was examined using ELISA. The interconnections among NEAT1, miR‐26a‐5p, and ROCK1 were confirmed using starbase, luciferase assay, and RIP.LPS treatment augmented NEAT1 and ROCK1 levels while mitigating miR‐26a‐5p level in BEAS‐2B cells. Additionally, LPS treatment facilitated cell death and cell pyroptosis, whereas NEAT1 silencing could reverse these effects in BEAS‐2B cells. Mechanistically, NEAT1 positively mediated ROCK1 expression by targeting miR‐26a‐5p. Furthermore, miR‐26a‐5p inhibitor offset NEAT1 depletion‐mediated suppressive effects on cell death and cell pyroptosis. ROCK1 upregulation decreased the inhibitory impacts produced by miR‐26a‐5p overexpression on cell death and cell pyroptosis. Our outcomes demonstrated NEAT1 could reinforce LPS‐induced cell death and cell pyroptosis by repressing the miR‐26a‐5p/ROCK1 axis, thereby worsening ALI caused by sepsis. Our data indicated NEAT1, miR‐26a‐5p, and ROCK1 might be biomarkers and target genes for relieving sepsis‐induced ALI.

show abstract

Section: Discussionmentioning

confidence: 62%

“…35 MiR-129/TAK1 axis plays a protective role in sepsis-induced ALI by regulating the NF-κB pathway. 36 Here, we initially confirmed ROCK1 was a downstream molecule of miR-26a-5p to mediate sepsis-induced ALI via influencing cell death and cell pyroptosis. ROCK1 is a critical molecule in the regulation of inflammatory response.…”

Section: Discussionmentioning

confidence: 62%

lncRNA NEAT1 mediates LPS‐induced pyroptosis of BEAS‐2B cells via targeting miR‐26a‐5p/ROCK1 axis

Fan

Ma²,

Tang

et al. 2023

The Kaohsiung J of Med Scie

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show abstract

“…For example, miR-326 could target TLR4 to mitigate sepsis-induced ALI [28]. MiR-129/TAK1 axis play a protective role in sepsisinduced ALI through regulating NF-κB pathway [29]. Here, we rstly con rmed ROCK1 was a downstream molecule of miR-26a-5p to mediate ALI via affecting cell apoptosis and in ammatory response.…”

Section: Discussionmentioning

confidence: 73%

LncRNA NEAT1 exacerbates sepsis-induced acute lung injury via targeting miR-26a-5p/ROCK1 axis

Fan

Tang

et al. 2022

Preprint

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Background: Acute lung injury (ALI) is a severe disease of respiratory system, which one of the most common causes is sepsis induction. Cell apoptosis and inflammation contribute to the progression of ALI and lncRNAs play crucial roles in ALI. Hence, this study is to unearth the specific mechanism of NEAT1.Methods: BEAS-2B cells was exposed to lipopolysaccharide (LPS) to construct cell model of sepsis-induced ALI. The gene and protein expression were evaluated using qRT-PCR and western blot. Cell viability was determined by CCK-8. Cell apoptosis was detected utilizing flow cytometry. The secretion of inflammatory factors was assessed using ELISA. The interconnections among NEAT1, miR-26a-5p and ROCK1 were validated using starbase, luciferase assay and RIP.Results: LPS treatment elevated NEAT1 and ROCK1 levels while reduced miR-26a-5p level in BEAS-2B cells. Besides, LPS treatment augmented cell apoptosis and enhanced inflammatory cytokine secretion, whereas NEAT1 silencing could reversed LPS-mediated these influences in BEAS-2B cells. Mechanistically, NEAT1 positively mediated ROCK1 expression through targeting miR-26a-5p. Moreover, miR-26a-5p inhibitor offset NEAT1 depletion-mediated suppressive influences on cell apoptosis and inflammation. ROCK1 upregulation attenuated the inhibitory impacts generated by miR-26a-5p overexpression on cell apoptosis and inflammation. Conclusion: Our results revealed NEAT1 could reinforce LPS-induced cell apoptosis and inflammatory response through repressing miR-26a-5p/ROCK1 axis, thereby aggravating ALI caused by sepsis. Our data suggested NEAT1, miR-26a-5p and ROCK1 might be biomarkers and targets genes for alleviating sepsis-induced ALI.

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“…However, the molecular pathways behind such effects remain unclear [ 213 , 214 ]. More recently, miR-129 was discovered to exert its protective role by blocking the TAK1 and NF-κB pathways [ 215 ].…”

Section: Resultsmentioning

confidence: 99%

Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review

Maiese

Scatena

Costantino

et al. 2022

IJMS

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Sepsis is a critical condition characterized by increased levels of pro-inflammatory cytokines and proliferating cells such as neutrophils and macrophages in response to microbial pathogens. Such processes lead to an abnormal inflammatory response and multi-organ failure. MicroRNAs (miRNA) are single-stranded non-coding RNAs with the function of gene regulation. This means that miRNAs are involved in multiple intracellular pathways and thus contribute to or inhibit inflammation. As a result, their variable expression in different tissues and organs may play a key role in regulating the pathophysiological events of sepsis. Thanks to this property, miRNAs may serve as potential diagnostic and prognostic biomarkers in such life-threatening events. In this narrative review, we collect the results of recent studies on the expression of miRNAs in heart, blood, lung, liver, brain, and kidney during sepsis and the molecular processes in which they are involved. In reviewing the literature, we find at least 122 miRNAs and signaling pathways involved in sepsis-related organ dysfunction. This may help clinicians to detect, prevent, and treat sepsis-related organ failures early, although further studies are needed to deepen the knowledge of their potential contribution.

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MicroRNA‑129 plays a protective role in sepsis‑induced acute lung injury through the suppression of pulmonary inflammation via the modulation of the TAK1/NF‑κB pathway

Cited by 10 publications

References 58 publications

lncRNA NEAT1 mediates LPS‐induced pyroptosis of BEAS‐2B cells via targeting miR‐26a‐5p/ROCK1 axis

lncRNA NEAT1 mediates LPS‐induced pyroptosis of BEAS‐2B cells via targeting miR‐26a‐5p/ROCK1 axis

LncRNA NEAT1 exacerbates sepsis-induced acute lung injury via targeting miR-26a-5p/ROCK1 axis

Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review

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