The FASEB Journal · 2023 · 12 citations · 21 references
Life SciencesCardiologyMolecular BiologyGene ExpressionInflammationInnate ImmunityCardiovascular DiseaseNoncoding Rna BiologyNoncoding Rna FunctionRna InterferenceInduced CardiomyocytesLong Noncoding Rna-mediated Apoptosis ControlMechanisms Of Cardiac InjuryMyeloid Differentiation Primary Response 88 SignalingNoncoding Rna In ApoptosisNoncoding Rna-mediated EffectsPediatric Intensive Care SurgeStress Response By Noncoding Rna
Sepsis-induced myocardial depression (SIMD) is common in pediatric intensive care units and seriously threatens children's health. Recently, long noncoding RNAs (lncRNAs) have been showed to play important roles in various diseases; however, its role in SIMD is unclear. In this study, we used lipopolysaccharide (LPS)-treated rats and H9c2 cardiomyocytes to mimic SIMD in vivo and in vitro. We found that the expression of a novel lncRNA, we named lncRNA-AABR07066529.3, was elevated in LPS-induced rat heart tissue and H9c2 cardiomyocytes. In addition, LPS-induced inflammation, apoptosis, and pyroptosis were significantly exacerbated after lncRNA-AABR07066529.3 knockdown. Moreover, we found that myeloid differentiation factor 88 (MyD88) was upregulated in LPS-treated groups and was inhibited by lncRNA-AABR07066529.3. Besides, MyD88 knockdown abolished lncRNA-AABR07066529.3 silencing effects on inflammation, apoptosis, and pyroptosis induced by LPS in H9c2 cardiomyocytes. In our study, we found lncRNA-AABR07066529.3 exerted protective effects on LPS-induced cardiomyocytes by regulating MyD88 and might serve as a potential treatment target for SIMD.
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The Transcriptional Landscape of the Mammalian Genome
Piero Carninci, Takeya Kasukawa, Shintaro Katayama et al. · Science · 2005 · 3.6K citations