Long non-coding RNA OIP5-AS1 aggravates acute lung injury by promoting inflammation and cell apoptosis via regulating the miR-26a-5p/TLR4 axis

Sun, Qiang; Luo, Man; Gao, Zhiwei; Han, Xiaowei; Wu, Weiqin; Zhao, Hongmei

doi:10.1186/s12890-021-01589-1

Cited by 10 publications

(14 citation statements)

References 52 publications

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“…For example, in LPS-induced lung cells, miR-26a-5p upregulation could evidently prohibit cell apoptosis and in ammatory response [10,11]. A prior study proposed miR-26a-5p was lowered by LPS administration in mice and human lung cells or lung tissues of mice [11], implying miR-26a-5p was implicated in sepsis-induced ALI. Here, miR-26a-5p level was reduced in BEAS-2B cells upon LPS induction.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-26a-5p was extensively investigated in diverse diseases such as cardiac hypertrophy, gastric cancer, sepsis-induced ALI [10,24,25]. For example, in LPS-induced lung cells, miR-26a-5p upregulation could evidently prohibit cell apoptosis and in ammatory response [10,11]. A prior study proposed miR-26a-5p was lowered by LPS administration in mice and human lung cells or lung tissues of mice [11], implying miR-26a-5p was implicated in sepsis-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

“…Diverse microRNAs such as miR-147b, miR-486-5p were reported to be engaged in alleviating or deteriorating the progression of ALI through mediating cell apoptosis and in ammatory response [8,9]. Studies proposed miR-26a-5p played protective effects in sepsis-induced ALI [10,11], but its upstream and downstream molecular regulatory mechanisms remain to be further revealed.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…miR‐26a‐5p/IL‐6 axis alleviates sepsis‐induced acute kidney injury by inhibiting renal inflammation 28 . Overexpression of miR‐26a‐5p could alleviate acute lung injury by targeting TLR4 to reduce cellular inflammation 29 . Another previously study also reported that miR‐26a‐5p alleviates neuropathic pain in a rat model of CCI through decreasing the release of the inflammatory factors IL‐1β, IL‐6, and TNF‐α by targeting MAPK6 30 .…”

Section: Introductionmentioning

confidence: 91%

miR‐26a‐5p alleviates CFA‐induced chronic inflammatory hyperalgesia through Wnt5a/CaMKII/NFAT signaling in mice

Liu

Guo

et al. 2023

CNS Neurosci Ther

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Background: Inflammation often leads to the occurrence of chronic pain, and many miRNAs have been shown to play a key role in the development of inflammatory pain.However, whether miR-26a-5p relieves pain induced by inflammation and its possible mechanism are still unclear. Methods:The complete Freund's adjuvant (CFA)-induced inflammatory pain mouse model was employed. Intrathecal or subcutaneous injection of miR-26a-5p agomir was performed after modeling to study its antinociceptive effect and the comparison of different administration methods. Bioinformatics analysis of miRNAs was performed to study the downstream mechanisms of miR-26a-5p. HE staining, RT-qPCR, Western blotting, and immunofluorescence were used for further validation.Results: A single intrathecal and subcutaneous injection of miR-26a-5p both reversed mechanical hypersensitivity and thermal latency in the left hind paw of mice with CFA-induced inflammatory pain. HE staining and immunofluorescence studies found that both administrations of miR-26a-5p alleviated inflammation in the periphery and spinal cord. Bioinformatics analysis and dual-luciferase reporter gene analysis identified Wnt5a as a direct downstream target gene of miR-26a-5p. Wnt5a was mainly expressed in neurons and microglia in the spinal cord of mice with inflammatory pain.Intrathecal injection of miR-26a-5p could significantly reduce the expression level of Wnt5a and inhibit the downstream molecules of noncanonical Wnt signaling Camk2/ NFAT, inhibiting the release of spinal cord inflammatory factors and alleviating the activation of microglia. In addition, miR-26a-5p could also inhibit lipopolysaccharide (LPS)-stimulated BV2 cell inflammation in vitro through a noncanonical Wnt signaling pathway.Conclusions: miR-26a-5p is a promising therapy for CFA-induced inflammatory pain.Both intrathecal and subcutaneous injections provide relief for inflammatory pain. miR-26a-5p regulated noncanonical Wnt signaling to be involved in analgesia partly through antineuroinflammation, suggesting a pain-alleviating effect via noncanonical Wnt signaling pathway in the CFA-induced inflammatory pain model in vivo.

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“…Earlier studies have proved the possible role of lncRNAs in different respiratory diseases such as ALI [ 10 ], eosinophilic asthma [ 11 ], pneumonia [ 12 ], cigarette smoke-associated airway inflammatory disorder [ 13 ], etc. Crucial roles of lncRNAs have been identified in the pathogenesis of ALI [ 14 , 15 ]. LncRNAs not only possess a key role in the pathogenesis of ALI but also retain great potentials for the diagnosis [ 16 ] and treatment of ALI [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA: A Novel Insight into the Pathogenesis of Acute Lung Injury

Dutta

Zhu²,

Han³

et al. 2023

JCM

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Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), represent an acute stage of lung inflammation where the alveolar epithelium loses its functionality. ALI has a devastating impact on the population as it not only has a high rate of incidence, but also has high rates of morbidity and mortality. Due to the involvement of multiple factors, the pathogenesis of ALI is complex and is not fully understood yet. Long noncoding RNAs (lncRNAs) are a group of non-protein-coding transcripts longer than 200 nucleotides. Growing evidence has shown that lncRNAs have a decisive role in the pathogenesis of ALI. LncRNAs can either promote or hinder the development of ALI in various cell types in the lungs. Mechanistically, current studies have found that lncRNAs play crucial roles in the pathogenesis of ALI via the regulation of small RNAs (e.g., microRNAs) or downstream proteins. Undoubtedly, lncRNAs not only have the potential to reveal the underlying mechanisms of ALI pathogenesis but also serve as diagnostic and therapeutic targets for the therapy of ALI.

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Long non-coding RNA OIP5-AS1 aggravates acute lung injury by promoting inflammation and cell apoptosis via regulating the miR-26a-5p/TLR4 axis

Cited by 10 publications

References 52 publications

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

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

miR‐26a‐5p alleviates CFA‐induced chronic inflammatory hyperalgesia through Wnt5a/CaMKII/NFAT signaling in mice

Long Noncoding RNA: A Novel Insight into the Pathogenesis of Acute Lung Injury

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