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miR-93-3p alleviates lipopolysaccharide-induced inflammation and apoptosis in H9c2 cardiomyocytes by inhibiting toll-like receptor 4.
Tang, Bi; Xuan, Ling; Tang, Mingming; Wang, Hongju; Zhou, Jing; Liu, Jinjun; Wu, Shili; Li, Miaonan; Wang, Xiaojing; Zhang, Heng.
Afiliación
  • Tang B; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Xuan L; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Tang M; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Wang H; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Zhou J; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Liu J; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Wu S; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Li M; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Wang X; Clinical and Basic Provincial Laboratory of Respiratory System Diseases of Anhui Province, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China.
  • Zhang H; Department of cardiovascular Medicine, The First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, Anhui Province, PR China. Electronic address: heng_zhangfh@sina.com.
Pathol Res Pract ; 214(10): 1686-1693, 2018 Oct.
Article en En | MEDLINE | ID: mdl-30195636
BACKGROUND: miR-93 is recently recognized to perform anti-inflammatory action in the pathological process of cardiomyocytes dysfunction. However, it remains unclear whether miR-93-3p involves in lipopolysaccharide (LPS)-induced inflammation and apoptosis in H9c2 cells. The present study aimed to investigate the functions of miR-93-3p and its target, toll-like receptor 4 (TLR4), in LPS-stimulated cardiomyocytes. MATERIAL AND METHODS: Cell viability was analyzed by CCK-8 assay. AnnexinV-FITC/PI staining and lactate dehydrogenase (LDH) assay were used to evaluate the cell death. The mRNA and protein levels were assayed by RT-qPCR and western blotting, respectively. The targeted gene was predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. RESULTS: LDH stimulation resulted in the suppression of cell viability and the increase in apoptosis rate, inflammatory cytokines and LDH levels, while inhibition of TLR4 with TAK-242 or overexpression of miR-93-3p dramatically blocked LPS-induced inflammation and apoptosis in cardiomyocytes. Intriguingly, bioinformatics analysis and experimental data suggested that TLR4 was a direct target of miR-93-3p, which could inhibit TLR4 expression by transfected with miR-93-3p mimics or elevate the expression of TLR4 by transfected with miR-93-3p inhibitors. Overexpression of TLR4 carried out an opposite effect to miR-93-3p and positively regulated LPS-induced inflammation and apoptosis in cardiomyocytes. CONCLUSION: miR-93-3p showed the protective effects against LPS-induced inflammation and apoptosis in cardiomyocytes by inhibiting TLR4 expression.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación de la Expresión Génica / Miocitos Cardíacos / MicroARNs / Receptor Toll-Like 4 Límite: Animals Idioma: En Revista: Pathol Res Pract Año: 2018 Tipo del documento: Article Pais de publicación: Alemania
Texto completo
Añadir a Mi BVS
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación de la Expresión Génica / Miocitos Cardíacos / MicroARNs / Receptor Toll-Like 4 Límite: Animals Idioma: En Revista: Pathol Res Pract Año: 2018 Tipo del documento: Article Pais de publicación: Alemania