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Bone morphogenetic protein signalling in airway epithelial cells during regeneration

机译：气道上皮细胞再生过程中骨形态发生蛋白信号转导

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Mechanisms of lung regeneration after injury remain poorly understood. Bone morphogenetic protein 4 (BMP4) is critical for lung morphogenesis and regulates differentiation of the airway epithelium during development, although its mechanism of action is unknown. The role of BMPs in adult lungs is unclear. We hypothesised that BMP signalling is involved in regeneration of damaged adult airways after injury. Our aims were to characterise the regeneration process in 1-nitronaphthalene (1-NN) injured airways, to determine if and when BMP signalling is activated during this process and investigate the effects of BMP4 on normal adult airway epithelial cells (AECs). Rats were injected with 50. mg/kg 1-NN and protein expression in AECs was examined by Western blotting of lung lysis lavage, and by immunofluorescence, at 6, 24, 48 and 96. h post injection. Expression of signalling molecules p-ERK-1, p-ERK-2 and p-Smad1/5/8 in AECs peaked at 6. h post injection, coincident with maximal inflammation and prior to airway denudation which occurred at 24. h. While airways were re-epithelialised by 48. h, AEC proliferation peaked later at 96. h post 1-NN injection. In vitro, BMP4 induced a mesenchymal-like morphology in normal AECs, downregulated E-cadherin expression and increased migration in a wound closure assay. Thus, following acute injury, increased BMP signalling in AECs coincides with inflammation and precedes airway denudation and re-epithelialisation. Our data indicate that, similar to its role in controlling tissue architecture during development, BMP signalling regulates regeneration of the airways following acute injury, involving downregulation of E-cadherin and induction of migration in AECs.
机译：受伤后肺再生的机制仍知之甚少。骨形态发生蛋白4（BMP4）对于肺形态发生至关重要，并在发育过程中调节气道上皮的分化，尽管其作用机理尚不清楚。 BMP在成人肺中的作用尚不清楚。我们假设BMP信号传导与受伤后成年受损气道的再生有关。我们的目的是表征1-硝基萘（1-NN）受损气道的再生过程，确定在此过程中是否激活BMP信号以及何时激活BMP信号，并研究BMP4对正常成人气道上皮细胞（AEC）的影响。在注射后6、24、48和96小时，给大鼠注射50.mg/kg的1-NN，并通过Western印迹检测肺溶解灌洗液并通过免疫荧光检查AEC中的蛋白表达。信号分子p-ERK-1，p-ERK-2和p-Smad1 / 5/8在AEC中的表达在注射后6 h达到峰值，与最大炎症同时发生，并在24 h发生气道剥脱之前。当气道在48小时后重新上皮化时，ANN的增殖在1-NN注射后的96. h达到峰值。在体外，在伤口闭合试验中，BMP4诱导正常AEC中的间充质样形态，下调E-钙粘蛋白表达并增加迁移。因此，急性损伤后，AEC中BMP信号的增加与炎症同时发生，并在气道剥脱和再上皮形成之前发生。我们的数据表明，与其在发育过程中控制组织结构的作用类似，BMP信号传导在急性损伤后调节气道的再生，涉及E-钙粘蛋白的下调和在AEC中的迁移诱导。

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