PDF(Pubmed)
Abstract：
UNASSIGNED: Oral submucous fibrosis (OSF) is a fibrotic disease with high transformation of malignant disorders. Aberrant expression of lncRNA nuclear enriched abundant transcript 1 (NEAT1) was engaged with various fibrosis models, but its mechanism in OSF remained elusive.
UNASSIGNED: Fibrous buccal mucosa fibroblasts (fBMFs) were from OSF specimens. Myofibroblast activities including the alpha smooth muscle actin (α-SMA) distribution and invasion capacities were determined by Immunocytochemistry and Transwell assays. Gene and protein were identified by quantitative real time polymerase chain reaction or western blotting. Binding relationship was analyzed via Starbase and dual-luciferase reporter or RNA immunoprecipitation assays.
UNASSIGNED: NEAT1 and Tropomyosin-1 (TPM1) were significantly increased in OSF specimens, but miR-760 was decreased. NEAT1 knockdown repressed myofibroblast activities and reduced the fibrosis and Wnt/β-catenin pathway via miR-760/TPM1 axis. MiR-760 inhibition could reverse the regulation of NEAT1 knockdown via TPM1 in fBMFs.
UNASSIGNED: NEAT1 knockdown inhibited myofibroblast activities and Wnt/β-catenin pathway via miR-760/TPM1 axis in fBMFs. NEAT1 could be the target for inhibiting myofibroblast activities in fBMFs for OSF treatment.
UNASSIGNED: Fibrous buccal mucosa fibroblasts (fBMFs) were from OSF specimens. Myofibroblast activities including the alpha smooth muscle actin (α-SMA) distribution and invasion capacities were determined by Immunocytochemistry and Transwell assays. Gene and protein were identified by quantitative real time polymerase chain reaction or western blotting. Binding relationship was analyzed via Starbase and dual-luciferase reporter or RNA immunoprecipitation assays.
UNASSIGNED: NEAT1 and Tropomyosin-1 (TPM1) were significantly increased in OSF specimens, but miR-760 was decreased. NEAT1 knockdown repressed myofibroblast activities and reduced the fibrosis and Wnt/β-catenin pathway via miR-760/TPM1 axis. MiR-760 inhibition could reverse the regulation of NEAT1 knockdown via TPM1 in fBMFs.
UNASSIGNED: NEAT1 knockdown inhibited myofibroblast activities and Wnt/β-catenin pathway via miR-760/TPM1 axis in fBMFs. NEAT1 could be the target for inhibiting myofibroblast activities in fBMFs for OSF treatment.
摘要：
■口腔粘膜下纤维化(OSF)是一种恶性疾病高度转化的纤维化疾病。lncRNA核富集丰富转录物1（NEAT1）的异常表达与各种纤维化模型有关，但其在OSF中的机制仍然难以捉摸。
■纤维颊粘膜成纤维细胞(fBMF)来自OSF标本。通过免疫细胞化学和Transwell测定确定肌成纤维细胞活性，包括α平滑肌肌动蛋白（α-SMA）分布和侵袭能力。通过定量实时聚合酶链反应或蛋白质印迹鉴定基因和蛋白质。通过Starbase和双荧光素酶报告基因或RNA免疫沉淀测定分析结合关系。
■NEAT1和原肌球蛋白-1(TPM1)在OSF标本中显著增加,但是miR-760降低了。NEAT1敲低抑制肌成纤维细胞活性并通过miR-760/TPM1轴降低纤维化和Wnt/β-catenin途径。miR-760抑制可以逆转fBMF中通过TPM1对NEAT1敲低的调节。
■NEAT1敲低通过miR-760/TPM1轴抑制fBMF中的成肌纤维细胞活性和Wnt/β-catenin通路。NEAT1可能是抑制fBMF中肌成纤维细胞活性的靶标，用于OSF治疗。
■纤维颊粘膜成纤维细胞(fBMF)来自OSF标本。通过免疫细胞化学和Transwell测定确定肌成纤维细胞活性，包括α平滑肌肌动蛋白（α-SMA）分布和侵袭能力。通过定量实时聚合酶链反应或蛋白质印迹鉴定基因和蛋白质。通过Starbase和双荧光素酶报告基因或RNA免疫沉淀测定分析结合关系。
■NEAT1和原肌球蛋白-1(TPM1)在OSF标本中显著增加,但是miR-760降低了。NEAT1敲低抑制肌成纤维细胞活性并通过miR-760/TPM1轴降低纤维化和Wnt/β-catenin途径。miR-760抑制可以逆转fBMF中通过TPM1对NEAT1敲低的调节。
■NEAT1敲低通过miR-760/TPM1轴抑制fBMF中的成肌纤维细胞活性和Wnt/β-catenin通路。NEAT1可能是抑制fBMF中肌成纤维细胞活性的靶标，用于OSF治疗。
