Long noncoding RNA &amp;lt;italic&amp;gt;GAS5&amp;lt;/italic&amp;gt; attenuates cigarettesmoke-induced airway remodeling by regulatingmiR-217-5p/PTEN axis

Du, Yong; Ding, Yi; Shi, Tianyun; He, Wei; Feng, Jing; Mei, Zhoufang; Chen, Xuru; Feng, Xintong; Zhang, Xiaohua; Zhang, Jie

doi:10.3724/abbs.2022074

Cited by 8 publications

(7 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, we determined miR‐494‐3p expression in tissues and cells, and the results showed that smoke exposure and CSE treatment elevated miR‐494‐3p expression in lung tissues and cells and inhibition of KLF9 significantly downregulated miR‐494‐3p expression ( p < .05, Figure 3D). The downstream target genes of miR‐494‐3p were predicted by the TargetScan, miRWalk, and miRTarBase databases, and intersections of genes were identified (Figure 3E), among which the weak expression of PTEN in COPD has been previously documented 27,28 . The dual‐luciferase assay showed that the binding of miR‐494‐3p mimic to PTEN 3′UTR sequence inhibited luciferase activity ( p < .05, Figure 3F).…”

Section: Resultsmentioning

confidence: 68%

“…The downstream target genes of miR-494-3p were predicted by the TargetScan, miRWalk, and miR-TarBase databases, and intersections of genes were identified (Figure 3E), among which the weak expression of PTEN in COPD has been previously documented. 27,28 The dual-luciferase assay showed that the binding of miR-494-3p mimic to PTEN 3′UTR sequence inhibited luciferase activity (p < .05, Figure 3F). Additionally, the expression trend of PTEN in tissues and cells was opposite to that of miR-494-3p (p < .05, Figure 3G,H).…”

Section: Klf9 Promotes Mir-494-3p Expression To Repress Pten Expressionmentioning

confidence: 99%

See 1 more Smart Citation

Mechanism of KLF9 in airway inflammation in chronic obstructive pulmonary

Gu,

Wang,

et al. 2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

BackgroundChronic obstructive pulmonary disease (COPD) is an airway‐associated lung disorder, resulting in airway inflammation. This article aimed to explore the role of the krüppel‐like factor 9 (KLF9)/microRNA (miR)‐494‐3p/phosphatase and tensin homolog (PTEN) axis in airway inflammation and pave a theoretical foundation for the treatment of COPD.MethodsThe COPD mouse model was established by exposure to cigarette smoke, followed by measurements of total cells, neutrophils, macrophages, and hematoxylin and eosin staining. The COPD cell model was established on human lung epithelial cells BEAS‐2B using cigarette smoke extract. Cell viability was assessed by cell counting kit‐8 assay. miR‐494‐3p, KLF9, PTEN, and NLR family, pyrin domain containing 3 (NLRP3) levels in tissues and cells were measured by quantitative real‐time polymerase chain reaction or Western blot assay. Inflammatory factors (TNF‐α/IL‐6/IL‐8/IFN‐γ) were measured by enzyme‐linked immunosorbent assay. Interactions among KLF9, miR‐494‐3p, and PTEN 3′UTR were verified by chromatin immunoprecipitation and dual‐luciferase assays.ResultsKLF9 was upregulated in lung tissues of COPD mice. Inhibition of KLF9 alleviated airway inflammation, reduced intrapulmonary inflammatory cell infiltration, and repressed NLRP3 expression. KLF9 bound to the miR‐494‐3p promoter and increased miR‐494‐3p expression, and miR‐494‐3p negatively regulated PTEN expression. miR‐494‐3p overexpression or Nigericin treatment reversed KLF9 knockdown‐driven repression of NLRP3 inflammasome and inflammation.ConclusionKLF9 bound to the miR‐494‐3p promoter and repressed PTEN expression, thereby facilitating NLRP3 inflammasome‐mediated inflammation.

show abstract

Section: Resultsmentioning

confidence: 68%

Section: Klf9 Promotes Mir-494-3p Expression To Repress Pten Expressionmentioning

confidence: 99%

Mechanism of KLF9 in airway inflammation in chronic obstructive pulmonary

Gu,

Wang,

et al. 2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

show abstract

“…22 lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR-223-3p/ NLRP3 axis. 23 Many studies have also confirmed the expression profile of lncRNA in the lung tissues of non-smokers and smokers, with or without COPD, 24 which will help to find early biomarkers and treatment targets associated with COPD. 13 Differential gene expression of LINC00599 has been reported in current smokers as compared to former smokers, and up-regulation of LINC00599 was indicated in response to cigarette smoking.…”

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

Dong

2022

Hum Exp Toxicol

View full text Add to dashboard Cite

LINC00599 has been reported to be upregulated in response to cigarette smoking. However, the effect and underlying mechanism of LINC00599 in chronic obstructive pulmonary disease (COPD) are still under exploration. In this study, LINC00599 was upregulated in the COPD patients and was of clinical value to distinguish COPD patients. COPD cell models were established using 16HBE cells under cigarette smoke extract (CSE) treatment. LINC00599 levels were elevated in a dose and time-dependent way in response to CSE stimulation. The effect of LINC00599 on CSE-induced 16HBE cells was explored. The results showed that LINC00599 deficiency reversed the CSE-induced inhibition on cell viability and proliferation, and rescued the CSE-induced enhancement on cell 16HBE cell apoptosis and inflammation response. Moreover, LINC00599 bound with miR-212-5p to upregulate the BASP1 (brain abundant membrane attached signal protein 1) expression. MiR-212-5p was expressed at a low level in the tissue samples of COPD patients, and its levels were upregulated in LINC00599 silenced cells. BASP1 was targeted by miR-212-5p and its upregulation was identified in the tissue samples of COPD patients and cell models. BASP1 levels were downregulated after miR-212-5p overexpression or LINC00599 silencing. Moreover, the rescue assays demonstrated that BASP1 overexpression reversed the effect of silenced LINC00599 on 16HBE cells after CSE treatment, which indicated that LINC00599 promoted the COPD development by regulating BASP1 expression. In conclusion, LINC00599 facilitated CSE-induced cell apoptosis and inflammation response, while inhibiting the cell viability and proliferation in COPD progression via modulating miR-212-5p/BASP1 axis.

show abstract

“…Referring to previous studies, 10 cigarettes were ignited, and the smoke bubbled through 30 mL of DMEM medium [ 22 ]. After the suspension was filtered and the pH was adjusted to 7.4, the solution is defined as the stock solution, i.e., 100% concentration.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA SNHG4 aggravates cigarette smoke-induced COPD by regulating miR-144-3p/EZH2 axis

Song,

Chen

2023

BMC Pulm Med

View full text Add to dashboard Cite

Objective The purpose of this study was to explore the expression level of SNHG4 in patients with COPD and its diagnostic value in COPD, to probe the biological function of SNHG4 in COPD at the cellular level, and to reveal the interaction between SNHG4 and miR-144-3p/EZH2 axis. Methods The serum levels of SNHG4, miR-144-3p and EZH2 in healthy people and patients with COPD were detected by RT-qPCR. The diagnostic value of SNHG4 in COPD was evaluated by ROC curve. Pearson method was chosen to estimate the correlation between SNHG4 and clinical indicators in patients with COPD. Cigarette smoke extract (CSE) was obtained, and Beas-2B cells were exposed with 2% CSE to establish an inflammatory cell model of COPD in vitro. MTT assay was used to detect cell viability, flow cytometry was used to evaluate cell apoptosis, and ELISA was performed to detect inflammatory cytokines. Dual-luciferase reporting assay was carried out to verify the targeting of lncRNA-miRNA or miRNA-mRNA. Results (1) The expression of SNHG4 is decreased in patients with COPD, and the expression level in acute exacerbation COPD was lower than that in stable COPD. SNHG4 demonstrated high diagnostic accuracy in distinguishing between stable and acute exacerbation COPD. (2) The expression of SNHG4 was decreased in CSE-induced Beas-2B cells, and overexpression of SNHG4 was beneficial to alleviate CSE-induced apoptosis and inflammation. (3) The expression of miR-144-3p is up-regulated in patients with COPD and CSE-induced Beas-2B cells. MiR-144-3p has a targeting relationship with SNHG4, which is negatively regulated by SNHG4. Overexpression of miR-144-3p could counteract the beneficial effects of increased SNHG4 on CSE-induced cells. (4) The expression of EZH2 is reduced in patients with COPD and CSE-induced Beas-2B cells. Bioinformatics analysis and luciferase reporter gene confirmed that EZH2 is the downstream target gene of miR-144-3p and is negatively regulated by miR-144-3p. Conclusion The expression of SNHG4 decreased in patients with COPD, and it may promote the progression of COPD by inhibiting the viability, promoting apoptosis and inflammatory response of bronchial epithelial cells via regulating the miR-144-3p/EZH2 axis.

show abstract

Long noncoding RNA <italic>GAS5</italic> attenuates cigarettesmoke-induced airway remodeling by regulatingmiR-217-5p/PTEN axis

Cited by 8 publications

References 28 publications

Mechanism of KLF9 in airway inflammation in chronic obstructive pulmonary

Mechanism of KLF9 in airway inflammation in chronic obstructive pulmonary

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

Long non-coding RNA SNHG4 aggravates cigarette smoke-induced COPD by regulating miR-144-3p/EZH2 axis

Contact Info

Product

Resources

About