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Войти в исследования Anatolian journal of cardiology · 2024
LncRNA TUG1 Knockdown Reduces Cardiomyocyte Damage in Viral Myocarditis by Targeting the miR-140-3p/CXCL8 Axis.
СтатьяНазвание и аннотация: Перевод в очереди
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Shi Ji, Sun Qiyin
Аннотация
BACKGROUND: The purpose of this study was to probe the specific role of long noncoding RNA taurine upregulation 1 (LncRNA TUG1) in viral myocarditis (VMC).
METHODS: The mouse model of VMC was induced by Coxsackievirus type B3 (CVB3). LncRNA TUG1 was subsequently silenced, and micro-140-3p (miR-140-3p) was overexpressed in VMC mice. GenePharma synthesized wild-type and mutant LncRNA TUG1 or CXCL8 (C-X-C Motif Chemokine Ligand 8, Interleukin-8) fragments containing the miR-140-3p binding site and cloned them into the pmirGLO luciferase reporter vector. Dual luciferase reporter assays were performed to test the activity of LncRNA TUG1 or CXCL8 fragments containing miR-140-3p mimic and mimic NC. The effects of silencing LncRNA TUG1 on cell proliferation, apoptosis, and inflammation in the VMC mouse model and in vitro were investigated by flow cytometry, enzyme linked immunosorbent assay, and western blot.
RESULTS: In the VMC mouse model, LncRNA TUG1 and CXCL8 were upregulated, while miR-140-3p was downregulated. Suppressing LncRNA TUG1 led to inhibition of CXCL8 by promoting miR-140-3p. Suppressing LncRNA TUG1 or CXCL8 or restoring miR-140-3p were observed to increase cell viability and decrease apoptosis rate of cardiomyocytes.
CONCLUSION: LncRNA TUG1 knockdown suppresses inflammation and damage of VMC cardiomyocytes via the miR-140-3p/CXCL8 axis.
METHODS: The mouse model of VMC was induced by Coxsackievirus type B3 (CVB3). LncRNA TUG1 was subsequently silenced, and micro-140-3p (miR-140-3p) was overexpressed in VMC mice. GenePharma synthesized wild-type and mutant LncRNA TUG1 or CXCL8 (C-X-C Motif Chemokine Ligand 8, Interleukin-8) fragments containing the miR-140-3p binding site and cloned them into the pmirGLO luciferase reporter vector. Dual luciferase reporter assays were performed to test the activity of LncRNA TUG1 or CXCL8 fragments containing miR-140-3p mimic and mimic NC. The effects of silencing LncRNA TUG1 on cell proliferation, apoptosis, and inflammation in the VMC mouse model and in vitro were investigated by flow cytometry, enzyme linked immunosorbent assay, and western blot.
RESULTS: In the VMC mouse model, LncRNA TUG1 and CXCL8 were upregulated, while miR-140-3p was downregulated. Suppressing LncRNA TUG1 led to inhibition of CXCL8 by promoting miR-140-3p. Suppressing LncRNA TUG1 or CXCL8 or restoring miR-140-3p were observed to increase cell viability and decrease apoptosis rate of cardiomyocytes.
CONCLUSION: LncRNA TUG1 knockdown suppresses inflammation and damage of VMC cardiomyocytes via the miR-140-3p/CXCL8 axis.