Long noncoding RNA MIR3142HG accelerates lipopolysaccharide-induced acute lung injury via miR-95-5p/JAK2 axis

Gao, Yanqiu; Li, Shuangfeng; Dong, Rui; Li, Xiaoyan

doi:10.1007/s13577-022-00687-4

Cited by 6 publications

(3 citation statements)

References 41 publications

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“…LncRNA MIR3142HG has been determined to mediate LPSinduced ALI in human pulmonary microvascular endothelial cells (HPMECs) by targeting the miR-450b-5p/HMGB1 axis, especially in accelerating apoptotic and inflammatory responses [48]. Another research study has further confirmed the overexpression of MIR3142HG in ALI patients, while also showing that the MIR3142HG/miR-95-5p/JAK2 axis might aggravate the progression of LPS-induced ALI in HPMEC and A549 cells [49]. These results indicated that MIR3142HG might be a potential ALI biomarker.…”

Section: Discussionmentioning

confidence: 97%

Insight into the lncRNA–mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury

Shen

Gong

et al. 2023

CIMB

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Long non-coding RNAs (lncRNAs) participate in acute lung injury (ALI). However, their latent biological function and molecular mechanism have not been fully understood. In the present study, the global expression profiles of lncRNAs and mRNAs between the control and lipopolysaccharide (LPS)-stimulated groups of human normal lung epithelial cells (BEAS-2B) were determined using high-throughput sequencing. Overall, a total of 433 lncRNAs and 183 mRNAs were differentially expressed. A lncRNA–mRNA co-expression network was established, and then the top 10 lncRNAs were screened using topological methods. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis results showed that the key lncRNAs targeting mRNAs were mostly enriched in the inflammatory-related biological processes. Gene set variation analysis and Pearson’s correlation coefficients confirmed the close correlation for the top 10 lncRNAs with inflammatory responses. A protein–protein interaction network analysis was conducted based on the key lncRNAs targeting mRNAs, where IL-1β, IL-6, and CXCL8 were regarded as the hub genes. A competing endogenous RNA (ceRNA) modulatory network was created with five lncRNAs, thirteen microRNAs, and twelve mRNAs. Finally, real-time quantitative reverse transcription-polymerase chain reaction was employed to verify the expression levels of several key lncRNAs in BEAS-2B cells and human serum samples.

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Section: Discussionmentioning

confidence: 97%

Insight into the lncRNA–mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury

Shen

Gong

et al. 2023

CIMB

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“…LncRNA is commonly researched in human disorders, such as diseases of the respiratory system. LncRNA CASC2 is down‐regulated, lncRNA MALAT1 is up‐regulated, and lncRNA MIR3142HG is overexpressed in patients with ALI, indicating that their expression may be influenced by the occurrence of ALI 18–20 . The content of UCA1 is elevated and related to the disease severity and prognosis in patients with sepsis, which may become the cause of ALI 21 .…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA CASC2 is down‐regulated, lncRNA MALAT1 is up‐regulated, and lncRNA MIR3142HG is overexpressed in patients with ALI, indicating that their expression may be influenced by the occurrence of ALI. 18 , 19 , 20 The content of UCA1 is elevated and related to the disease severity and prognosis in patients with sepsis, which may become the cause of ALI. 21 In the pneumonia models constructed using ligation and puncture and lipopolysaccharide, the levels of UCA1 are increased, and it can aggravate the development of pneumonia.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the prognostic value of lncRNA UCA1 combined with extravascular lung water index and lung ultrasound score in patients with acute lung injury

Jiang

et al. 2023

Clinical Respiratory J

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Introduction Acute lung injury (ALI) is a common and rapidly developing critical inflammatory lung disease in clinic. This study investigated the predictive value of lncRNA UCA1, extravascular lung water index (EVLWI), and lung ultrasound score (LUS) in predicting the overall outcome of patients with ALI. Methods Patients with ALI were recruited for detecting the content of UCA1, EVLWI, and LUS. All patients were cataloged into the survival group and death group according to the prognosis. The discrepancy of UCA1, EVLWI, and LUS was compared in the two groups. The prognostic significance of UCA1, EVLWI, LUS, and their combination was estimated by logistic regression and the receiver operating characteristic (ROC) curve. Results The levels of UCA1, LUS, and EVLWI were elevated in the death group compared with the survival group. The content of UCA1 was positively correlated with LUS scores and EVLWI scores. UCA1, LUS, and EVLWI were independent indicators of predicting the prognosis of patients with ALI. The ROC curve reflected that UCA1, LUS, and EVLWI could forecast the endpoint events of patients with ALI whereas their combined approach had the highest accuracy. Conclusion Highly expressed UCA1 is a biomarker in forecasting the outcome of patients with ALI. It had high accuracy in predicting the endpoint of patients with ALI when combined with LUS and EVLWI.

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Inhibition of gp130 alleviates LPS-induced lung injury by attenuating apoptosis and inflammation through JAK1/STAT3 signaling pathway

Wang

et al. 2023

Inflamm. Res.

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Long noncoding RNA MIR3142HG accelerates lipopolysaccharide-induced acute lung injury via miR-95-5p/JAK2 axis

Cited by 6 publications

References 41 publications

Insight into the lncRNA–mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury

Insight into the lncRNA–mRNA Co-Expression Profile and ceRNA Network in Lipopolysaccharide-Induced Acute Lung Injury

Evaluation of the prognostic value of lncRNA UCA1 combined with extravascular lung water index and lung ultrasound score in patients with acute lung injury

Inhibition of gp130 alleviates LPS-induced lung injury by attenuating apoptosis and inflammation through JAK1/STAT3 signaling pathway

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