Objective:To clarify the effect of long non-coding RNA MALAT1 on the activation ability of buccal mucosal fibroblasts(BMFs)induced by arecoline,and to establish theoretical basis for a new therapeutic pathway to oral submucous fibrosis(OSF).Methods:BMFs were cultured in vitro,and were stimulated with different concen-trations of arecoline to construct OSF-disease models at the cellular level.CCK-8 method was used to detect cell via-bility.BMFs activation was detected by Transwell method and collagen gel shrinkage method.Quantitative real-time PCR(qRT-PCR)was used to detect the expression of α-smooth muscle actin antibody(α-SMA)and lncRNA MALAT1 in BMFs.siRNA-MALATl was transiently transfected into BMFs to assess changes in the migration and contraction capacity of BMFs stimulated by arecoline.Results:10 μg/mL of arecoline was the optimal concentration for constructing OSF-disease models in vitro,when intracellular expression of α-SMA and lncRNA MALAT1 was elevated.Trans well experiments and collagen gel contraction experiments suggested that knockdown lncRNA MALAT inhibited arecoline-induced BMFs contraction and migration.Conclusion:lncRNA MALAT1 plays an important role in arecoline-induced BMFs activation,cell contraction,and mi-gration.
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