ArticleImmunity, inflammation and disease2021
lncRNA Mirt2 upregulates miR-1246 through methylation to suppress LPS-induced lung cell apoptosis.
Article in Immunity, inflammation and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- LncRNA Mirt2 Attenuates Osteoarthritis Progression by Promoting miR-429/TBK1-Mediated Autophagy.Immunity, inflammation and disease · 2026Article
- Macrophage-derived long non-coding RNAs in cancer: pioneering targets for immune modulation and personalized therapy.Frontiers in immunology · 2026Review
- Implications of Protein Posttranslational Modifications in Sepsis-Induced Acute Lung Injury and Acute Respiratory Distress Syndrome.Shock (Augusta, Ga.) · 2025Review
- PARP3 promotes macrophage inflammation via mono ADP ribosylation of Ppia Glu140.Molecular medicine (Cambridge, Mass.) · 2025Article
- Article
- Apoptotic extracellular vesicles derived from hypoxia-preconditioned mesenchymal stem cells within a modified gelatine hydrogel promote osteochondral regeneration by enhancing stem cell activity and regulating immunity.Journal of nanobiotechnology · 2024Article
- lncRNA Mirt2 upregulates miR-1246 through methylation to suppress LPS-induced lung cell apoptosis.Immunity, inflammation and disease · 2021Article
- Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis.Frontiers in immunology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLong noncoding RNA Mirt2 has been proven to be a suppressor of lipopolysaccharide (LPS) (a key player in sepsis)-induced inflammation responses. Therefore, Mirt2 may also participate in sepsis. This study was carried out to analyze the interactions between Mirt2 and microRNA-1246 (miR-1246) in sepsis, with a specific focus on sepsis-induced acute lung injury (sepsis-ALI).
methodsForty sepsis patients (sepsis group; 23 males and 17 females; 40-65 years, 48.6 ± 6.3 years), 40 sepsis patients with acute lung injury (sepsis-ALI group, 23 males and 17 females; 40-65 years, 48.7 ± 6.4 years), and 40 healthy controls (control group, 23 males and 17 females; 40-65 years, 48.6 ± 6.1 years) were included. Mirt2 and miR-1246 expression in plasma samples from these patients were determined by a reverse transcription-quantitative polymerase chain reaction (PCR). Overexpression of Mirt2 and miR-1246 was achieved in human bronchial epithelial cells (HBEpCs) to explore the interaction between them. The effects of Mirt2 overexpression on miR-1246 methylation were analyzed by methylation-specific PCR. Cell apoptosis analysis was performed to analyze the role of Mirt2 and miR-1246 in the apoptosis of HBEpCs.
resultsMirt2 expression was downregulated in sepsis and was further downregulated in patients with sepsis-ALI. Mirt2 and miR-1246 found to be positively correlated. Downregulation of Mirt2 and miR-1246 was observed in HBEpCs with LPS treatment. In HBEpCs, Mirt2 overexpression increased miR-1246 expression but decreased its gene methylation. Cell apoptosis analysis showed that Mirt2 and miR-1246 negatively regulated the apoptosis of HBEpCs induced by LPS. In addition, miR-1246 inhibition reduced the inhibitory effects of Mirt2 overexpression on cell apoptosis.
conclusionsMirt2 may upregulate miR-1246 through methylation to suppress lung cell apoptosis.
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