Long Noncoding RNA AF131217.1 Regulated Coronary Slow Flow-Induced Inflammation Affecting Coronary Slow Flow via KLF4

• Autor(a) principal: Jiang,Haibing
• Data de Publicação: 2022
• Outros Autores: Ge,Zhengrong, Zhang,Lijing, Yang,Yi, Zhai,Xueqin, Chen,Zhanxi, Wei,Qing
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Brazilian Journal of Cardiovascular Surgery (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000400525
• topic: Myocardial Infarctation; Inflammation; Interleukin-18; Interleukin-6; RNA; Long Noncoding; C-Reactive Protein; MicroRNAs; GKLF protein

Abstract Introduction: This study investigated the correlation between the levels of long noncoding ribonucleic acids (lncRNAs) AF131217.1 and coronary slow flow (CSF). Methods: A total of 22 patients in the high-sensitivity C-reactive protein (hsCRP) group diagnosed with CSF from January 2018 to December 2018 were enrolled in this study. Coronary flow velocity was determined using the thrombolysis in myocardial infarction frame count (TFC) method. Results: LncRNA AF131217.1 expression in the CSF model was activated. Mean TFC was positively correlated with lncRNA AF131217.1 levels and hsCRP levels. LncRNA AF131217.1 induced inflammation factor levels in the in vitro model. Micro ribonucleic acid (miR)-128-3p is a target spot of lncRNA AF131217.1 on the inflammation in vitro model via Kruppel-like factor (KLF) 4. MiR-128-3p reduced inflammation factor levels (tumor necrosis factor alpha, interleukin [IL]-6, IL-1β, and IL-18). Conclusion: Thus, lncRNA AF131217.1 promoted inflammation in the regulated CSF via KLF4 by miR-128-3p.