FTO影响缺氧小鼠肺动脉平滑肌细胞迁移能力的研究
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南京医科大学第一附属医院

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CBX4在肺动脉高压中调控苏木化hnRNPs依赖的外泌体miRNAs分拣机制的研究


Effects of FTO on migration of pulmonary artery smooth muscle cells in hypoxic mice
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The first affiliated hospital with Nanjing medical university

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    摘要:

    目的 探究脂肪质量与肥胖相关蛋白(fat mass and obesity associated,FTO)是否影响缺氧小鼠肺动脉平滑肌细胞迁移能力。方法 体外培养小鼠肺动脉平滑肌细胞系(MPASMCs),用三气培养箱构建缺氧MPASMCs模型;免疫印迹实验用于检测FTO蛋白表达;FTO过表达以及敲除质粒转染MPASMCs以过表达或抑制FTO表达;细胞划痕实验检测细胞迁移能力。结果 缺氧培养后的MPASMCs中FTO蛋白表达明显下调,划痕实验提示细胞迁移加快,并在过表达FTO后明显减慢;常氧状态下敲低FTO表达出现了类似缺氧培养的“促迁移”表型。结论 在体外条件下MPASMCs缺氧培养后FTO蛋白水平下调,细胞迁移能力增强,并且FTO可能是促进MPASMCs迁移的关键调控基因。

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    Objective To investigate whether fat mass and obesity associated (FTO) protein affects the migration of pulmonary artery smooth muscle cells (PASMCs) in hypoxic mice. Methods Mouse pulmonary artery smooth muscle cells (MPASMCs) was cultured in vitro. The hypoxia model of MPASMCs was established in a three-gas incubator (37℃, 1%O2, 5%CO2). The expression of FTO protein was detected by Western blot. FTO overexpression and knockdown plasmids were transfected into MPASMCs to over-express or inhibit FTO expression. Cell Wound healing assay was used to detect cell migration ability. Results The expression of FTO protein in MPASMCs after hypoxia culture was significantly down-regulated. Scratch test indicated that MPASMCs migration was accelerated after hypoxia culture and was significantly slowed down after FTO was overexpressed in MPASMCs. Knockdown FTO expression in MPASMCs in normoxic state showed a "pro-migration" phenotype similar to hypoxic culture. Conclusions Under hypoxic conditions, the expression of FTO protein is down-regulated in MPASMCs and the cells migration ability is enhanced. FTO may be a key regulator of MPASMCs migration

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  • 收稿日期:2023-02-13
  • 最后修改日期:2023-03-17
  • 录用日期:2023-05-23
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