ArticleFrontiers in cell and developmental biology2020
Knockdown of lncRNA MALAT1 Alleviates LPS-Induced Acute Lung Injury via Inhibiting Apoptosis Through the miR-194-5p/FOXP2 Axis.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 61 citations in OpenAlex.
- Decoding the lncRNA-miRNA-mRNA network in sepsis-induced lung injury: from pathogenesis to extracellular vesicle-based therapy.Frontiers in immunology · 2026Review
- Inhibition of miR-194-5p avoids DUSP9 downregulation thus limiting sepsis-induced cardiomyopathy.Scientific reports · 2024Article
- HSPB8 attenuates lipopolysaccharide‑mediated acute lung injury in A549 cells by activating mitophagy.Molecular medicine reports · 2024Article
- GnRH-driven FTO-mediated RNA mBMC biology · 2024Article
- FOXP2 inhibits the aggressiveness of lung cancer cells by blocking TGFβ signaling.Oncology letters · 2024Article
- Photodynamic Therapy of LD4-Photosensitizer Attenuates the Acute Pneumonia Induced byACS pharmacology & translational science · 2024Article
- Pulmonary miRNA expression after polytrauma depends on the surgical invasiveness and displays an anti-inflammatory pattern by the combined inhibition of C5 and CD14.Frontiers in immunology · 2024Article
- MALAT1-mediated EZH2 Recruitment to the GFER Promoter Region Curbs Normal Hepatocyte Proliferation in Acute Liver Injury.Journal of clinical and translational hepatology · 2023Article
- Long Noncoding RNA: A Novel Insight into the Pathogenesis of Acute Lung Injury.Journal of clinical medicine · 2023Review
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- Role of Long Noncoding RNAs in the Regulation of Cellular Immune Response and Inflammatory Diseases.Cells · 2022Review
- LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis.BMC pulmonary medicine · 2022Article
- ROS-responsive polymer nanoparticles with enhanced loading of dexamethasone effectively modulate the lung injury microenvironment.Acta biomaterialia · 2022Article
- LncRNAMolecules (Basel, Switzerland) · 2022Article
- Knockdown of LncRNA MALAT1 Alleviates Coxsackievirus B3-Induced Acute Viral Myocarditis in Mice via Inhibiting Th17 Cells Differentiation.Inflammation · 2022Article
- The ROCK-ezrin signaling pathway mediates LPS-induced cytokine production in pulmonary alveolar epithelial cells.Cell communication and signaling : CCS · 2022Article
- MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44.Cell death discovery · 2022Article
- Long noncoding RNA Kcnq1ot1 prompts lipopolysaccharide-induced acute lung injury by microRNA-7a-5p/Rtn3 axis.European journal of medical research · 2022Article
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- Neutrophil extracellular traps mediate mInternational journal of biological sciences · 2022Article
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10 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
purposeWe aimed to identify and verify the key genes and lncRNAs associated with acute lung injury (ALI) and explore the pathogenesis of ALI. Research showed that lower expression of the lncRNA metastasis-associated lung carcinoma transcript 1 (MALAT1) alleviates lung injury induced by lipopolysaccharide (LPS). Nevertheless, the mechanisms of MALAT1 on cellular apoptosis remain unclear in LPS-stimulated ALI. We investigated the mechanism of MALAT1 in modulating the apoptosis of LPS-induced human pulmonary alveolar epithelial cells (HPAEpiC).
methodsDifferentially expressed lncRNAs between the ALI samples and normal controls were identified using gene expression profiles. ALI-related genes were determined by the overlap of differentially expressed genes (DEGs), genes correlated with lung, genes correlated with key lncRNAs, and genes sharing significantly high proportions of microRNA targets with MALAT1. Quantitative real-time PCR (qPCR) was applied to detect the expression of MALAT1, microRNA (miR)-194-5p, and forkhead box P2 (FOXP2) mRNA in 1 μg/ml LPS-treated HPAEpiC. MALAT1 knockdown vectors, miR-194-5p inhibitors, and ov-FOXP2 were constructed and used to transfect HPAEpiC. The influence of MALAT1 knockdown on LPS-induced HPAEpiC proliferation and apoptosis via the miR-194-5p/FOXP2 axis was determined using Cell counting kit-8 (CCK-8) assay, flow cytometry, and Western blotting analysis, respectively. The interactions between MALAT1, miR-194-5p, and FOXP2 were verified using dual-luciferase reporter gene assay.
resultsWe identified a key lncRNA (MALAT1) and three key genes (EYA1, WNT5A, and FOXP2) that are closely correlated with the pathogenesis of ALI. LPS stimulation promoted MALAT1 expression and apoptosis and also inhibited HPAEpiC viability. MALAT1 knockdown significantly improved viability and suppressed the apoptosis of LPS-stimulated HPAEpiC. Moreover, MALAT1 directly targeted miR-194-5p, a downregulated miRNA in LPS-stimulated HPAEpiC, when FOXP2 was overexpressed. MALAT1 knockdown led to the overexpression of miR-194-5p and restrained FOXP2 expression. Furthermore, inhibition of miR-194-5p exerted a rescue effect on MALAT1 knockdown of FOXP2, whereas the overexpression of FOXP2 reversed the effect of MALAT1 knockdown on viability and apoptosis of LPS-stimulated HPAEpiC.
conclusionOur results demonstrated that MALAT1 knockdown alleviated HPAEpiC apoptosis by competitively binding to miR-194-5p and then elevating the inhibitory effect on its target FOXP2. These data provide a novel insight into the role of MALAT1 in the progression of ALI and potential diagnostic and therapeutic strategies for ALI patients.
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