ArticleMammalian genome : official journal of the International Mammalian Genome Society2021
Knockdown of lncRNA LUCAT1 attenuates sepsis‑induced myocardial cell injury by sponging miR-642a.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2021. 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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8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Role of LncRNAs in the Pathogenesis of Sepsis and their Clinical Significance.Current molecular medicine · 2024Review
- Revealing Landscape of Competing Endogenous RNA Networks in Sepsis-Induced Cardiovascular Diseases.Reviews in cardiovascular medicine · 2023Review
- Inflammatory Genes Associated with Pristine Multi-Walled Carbon Nanotubes-Induced Toxicity in Ocular Cells.International journal of nanomedicine · 2023Article
- Protective effect and mechanism of γ-secretase inhibitor on myocardial injury in sepsis rats.American journal of translational research · 2023Article
- Construction of a potentially functional lncRNA-miRNA-mRNA network in sepsis by bioinformatics analysis.Frontiers in genetics · 2022Article
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis.Frontiers in immunology · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heart is one of the most common organs involved in sepsis-induced organ dysfunction and about 50% septic patients complicated with myocardial injury. So far, the molecular mechanisms underlying sepsis-induced cardiac damage remain unclear. In this study we aimed to evaluate the effect of miR-642a on sepsis-induced cardiac injury in vitro and explore the possible lncRNA-microRNA mechanism. We first downloaded GSE101639 to identify differentially expressed genes (DEGs) in sepsis. The expression of miR-642a in LPS-induced H9C2 cells was detected by qRT-PCR. MTT assay, cell migration, flow cytometry analysis, ELISA, qRT-PCR and Western blotting analysis were applied to evaluating the effect of miR-642a mimic on LPS-induced H9C2 cells. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. The results showed miR-642a expression was decreased in septic patients and LPS-induced H9C2 cells. Besides, MiR-642a mimic promoted cell viability and migration, inhibited cell apoptosis of LPS-induced H9C2 cells. Bioinformatics analysis showed miR-642a directly targets with 3'-UTR of ROCK1. Moreover, LUCAT1 regulated ROCK1 expression act as a competing endogenous RNA (ceRNA) for miR-642a. Our data demonstrated that lncRNA LUCAT1 could function via sponging miR-642a to regulate ROCK1 expression in LPS-induced H9C2 cells. And knockdown of lncRNA LUCAT1 could suppress LPS-induced cardiac injury in vitro.
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