ArticleCanadian respiratory journal2019
Overexpression of MALAT1 Relates to Lung Injury through Sponging miR-425 and Promoting Cell Apoptosis during ARDS.
Article in Canadian respiratory journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Exploring the translational landscape of the long noncoding RNA transcriptome in acute respiratory distress syndrome: it is a long way to the top.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Long Noncoding RNA: A Novel Insight into the Pathogenesis of Acute Lung Injury.Journal of clinical medicine · 2023Review
- Emerging role of long non-coding RNA MALAT1 related signaling pathways in the pathogenesis of lung disease.Frontiers in cell and developmental biology · 2023Review
- Long non-coding RNA (lncRNA): A potential therapeutic target in acute lung injury.Genes & diseases · 2022Review
- The expression profile of lung long non-coding RNAs and mRNAs in a mouse model of smoke inhalation injury.Bioengineered · 2022Article
- The lncRNAs/miR-30e/CHI3L1 Axis Is Dysregulated in Systemic Sclerosis.Biomedicines · 2022Article
- Article
- Focus on long non-coding RNA MALAT1: Insights into acute and chronic lung diseases.Frontiers in genetics · 2022Review
- Extracellular Vesicles, New Players in Sepsis and Acute Respiratory Distress Syndrome.Frontiers in cellular and infection microbiology · 2022Review
- PTEN: An Emerging Potential Target for Therapeutic Intervention in Respiratory Diseases.Oxidative medicine and cellular longevity · 2022Review
- Resveratrol inhibits cell apoptosis by suppressing long noncoding RNA (lncRNA) XLOC_014869 during lipopolysaccharide-induced acute lung injury in rats.Journal of thoracic disease · 2021Article
- lncRNA NEAT1 aggravates sepsis-induced lung injury by regulating the miR-27a/PTEN axis.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Long non-coding RNA review and implications in acute lung inflammation.Life sciences · 2021Review
- Effect and mechanism of phospholipid scramblase 4 (PLSCR4) on lipopolysaccharide (LPS)-induced injury to human pulmonary microvascular endothelial cells.Annals of translational medicine · 2021Article
- Comprehensive Analysis of the Profiles of Differentially Expressed mRNAs, lncRNAs, and circRNAs in Phosgene-Induced Acute Lung Injury.BioMed research international · 2021Article
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury during which severe inflammatory responses induce cell apoptosis, necrosis, and fibrosis. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a multiple function long noncoding RNA that was found overexpressed during acute lung injury. However, the roles of MALAT1 in ARDS patients are still unknown. Methods: Total RNA was extracted from the plasma, plasma exosome, and peripheral blood mononuclear cells (PBMCs) from 65 ARDS patients and 36 healthy controls. The MALAT1 and six candidate miRNAs levels were detected by qRT-PCR. The interaction between MALAT1 and miR-425 was predicted using a bioinformatics tool and verified by dual luciferase assay. Exosomes from ARDS patients were cultured with A549 and HFL-1 cells to confirm the delivery of miR-425 by exosomes. Cell apoptosis and viability were determined by flow cytometry and MTT assay. Results: We found MALAT1 was significantly increased in the ARDS patients' plasma and PBMCs. The MALAT1 level in PBMCs was negatively correlated with exosomal miR-425 level. MALAT1 interacted with miR-425 and protected phosphatase and tensin homolog (PTEN) expression in A549 and HFL-1 cells. Exosomes from ARDS patients delivered less miR-425 into A549 and HFL-1 cells and induced cell apoptosis via upregulating PTEN. Conclusion: This study identified increased MALAT1 and decreased miR-425 in ARDS patients and unveiled their roles during the pathogenesis of ARDS.
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