<scp>miR</scp>‐495 targets <scp>ROCK1</scp> to inhibit lipopolysaccharides‐induced <scp>WI</scp>‐38 cells apoptosis and inflammation

Zhang, Jian; Xiang, Jie; Liu, Ting; Wang, Xinwei; Tang, Ying; Liang, Yin

doi:10.1002/kjm2.12210

Cited by 12 publications

(8 citation statements)

References 38 publications

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“…Extracellular vesicles carrying Caspase-3 in lung epithelial cells with hyperoxia treatment aggravated in ammatory lung responses via activating ROCK1 pathway [30]. Additionally, ROCK1 could regulate cell viability, apoptosis, and in ammation in ALI [16,[32][33][34]. Here, our results revealed miR-26a-5p directly combined with ROCK1 and suppressed ROCK1 expression.…”

Section: Discussionmentioning

confidence: 55%

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: 55%

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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“…By using StarBase, the downstream genes of NEAT1 were screened, and the potential binding site between NEAT1 and miR-495 is presented in Figure 3a . Increasing evidence indicated that miR-495 acted as a vital regulator in the inflammation response of various diseases, such as pneumonia [ 22 ], inflammatory bowel disease [ 23 ], and ankylosing spondylitis [ 24 ]. Moreover, RT-qPCR analysis indicated that miR-495 expression was decreased in serum and middle ear effusion of OME ( Figure 3b ).…”

Section: Resultsmentioning

confidence: 99%

Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes the inflammation and apoptosis of otitis media with effusion through targeting microRNA (miR)-495 and activation of p38 MAPK signaling pathway

Dong

Huang

et al. 2021

Bioengineered

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Long non-coding RNA (lncRNA) plays a vital role in human inflammatory diseases. Our study aimed to investigate the function of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in otitis media with effusion (OME). The mRNA levels of NEAT1 and miR-495 were measured by RT-qPCR. The protein levels of p38 MAPK were detected by western blot. The levels of inflammatory cytokines were examined by ELISA. CCK-8 and flow cytometry assays were used to evaluate the cell viability and apoptosis, respectively. The interaction between NEAT1 and miR-495 was determined by luciferase reporter and RIP assays. NEAT1 was highly expressed in OME, and silencing of NEAT1 facilitated the cell proliferation and suppressed levels of inflammatory cytokines and cell apoptosis in LPS-induced HMEECs. Moreover, miR-495 was confirmed as a downstream target of NEAT1. Functional assays revealed that NEAT1 promoted the OME by targeting miR-495. It was further demonstrated that NEAT1 could activate the p38 MAPK signaling pathway by regulating miR-495, and the p38 MAPK inhibitor restored the effects of NEAT1 overexpression on the inflammation levels, cell proliferation, and apoptosis. Our study revealed that lncRNA NEAT1 served as a ceRNA to activate p38 MAPK signaling by targeting miR-495 in OME, which may offer a new target for OME treatment.

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“…37 Additionally, ROCK1 could regulate cell viability, apoptosis, and inflammation in ALI. 16,[38][39][40] Furthermore, Wang et al showed that ROCK1 could regulate cell pyroptosis to influence sepsis-induced acute kidney injury. 19 In our research, we determined that miR-26a-5p was directly combined with ROCK1 and suppressed ROCK1 expression.…”

Section: Discussionmentioning

confidence: 99%

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.

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miR‐495 targets ROCK1 to inhibit lipopolysaccharides‐induced WI‐38 cells apoptosis and inflammation

Cited by 12 publications

References 38 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

Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes the inflammation and apoptosis of otitis media with effusion through targeting microRNA (miR)-495 and activation of p38 MAPK signaling pathway

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

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