ArticleMolecular medicine (Cambridge, Mass.)2020
LncRNA LUADT1 sponges miR-195 to prevent cardiac endothelial cell apoptosis in sepsis.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- SNHG5 Exacerbates Sepsis-Induced Inflammatory Injury in Coronary Artery Endothelial Cells by Regulating METAP2-Mediated IL-8 Secretion.Mediators of inflammation · 2026Article
- Unveiling the Role of LncRNA in Sepsis-Associated Encephalopathy.Current medical science · 2025Review
- Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death.Journal of inflammation research · 2024Review
- Pim Kinases: Important Regulators of Cardiovascular Disease.International journal of molecular sciences · 2023Review
- Revealing Landscape of Competing Endogenous RNA Networks in Sepsis-Induced Cardiovascular Diseases.Reviews in cardiovascular medicine · 2023Review
- Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis.Frontiers in immunology · 2021Review
- The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction.Frontiers in cardiovascular medicine · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe oncogenic role of the newly identified lncRNA LUADT1 has been revealed in lung adenocarcinoma. It was reported that LUADT1 plays a critical role in multiple human diseases. This study was carried out to investigate the role of LUADT1 in sepsis.
methodsSixty patients with sepsis and sixty healthy volunteers were recruited for this study. Plasma samples were collected from all participants. Human primary coronary artery endothelial cells were also used in this study. The expression of Pim-1, miR-195 and LUADT1 were detected by RT-qPCR. The interaction between miR-195 and LUADT1 was determined by overexpression experiments and luciferase activity assay. Cell apoptosis was detected by flow cytometry. The expression of apoptosis-related protein was detected by Western blotting.
resultsBioinformatics analysis revealed the potential interaction between LUADT1 and miR-195, which was confirmed by dual luciferase reporter assay. LUADT1 was downregulated in patients with sepsis. Moreover, LPS treatment downregulated the expression of LUADT1 in primary cardiac endothelial cells. Overexpression of LUADT1 and miR-195 did not affect the expression of each other in primary cardiac endothelial cells. Interestingly, overexpression of LUADT1 was found to upregulate the expression of Pim-1, a target of miR-195. In addition, it was found that overexpression of LUADT1 and Pim-1 reduced the enhancement effects of miR-195 on LPS-induced cardiac endothelial cell apoptosis.
conclusionIn summary, LUADT1 may protect cardiac endothelial cells against apoptosis in sepsis by regulating the miR-195/Pim-1 axis.
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