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首页> 外文期刊>American Journal of Physiology >Pericytes contribute to airway remodeling in a mouse model of chronic allergic asthma
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Pericytes contribute to airway remodeling in a mouse model of chronic allergic asthma

机译：截瘫在慢性过敏性哮喘小鼠模型中有助于气道重塑

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Myofibroblast accumulation, subepithelial fibrosis, and vascular remodeling are complicating features of chronic asthma, but the mechanisms are not clear. Platelet-derived growth factors (PDGFs) regulate the fate and function of various mesenchymal cells and have been implicated as mediators of lung fibrosis. However, it is not known whether PDGF-BB signaling via PDGFRp, which is critical for the recruitment of pericytes to blood vessels, plays a role in airway remodeling in chronic asthma. In the present study, we used a selective PDGFR(S inhibitor (CP-673451) to investigate the role of PDGFRP signaling in the development of airway remodeling and lung dysfunction in an established mouse model of house dust mite-induced chronic allergic asthma. Unexpectedly, we found that pharmacological inhibition of PDGFR3 signaling in the context of chronic aeroallergen exposure led to exacerbated lung dysfunction and airway smooth muscle thickening. Further studies revealed that the inflammatory response to aeroallergen challenge in mice was associated with decreased PDGF-BB expression and the loss of pericytes from the airway microvasculature. In parallel, cells positive for pericyte markers accumulated in the subepithelial region of chronically inflamed airways. This process was exacerbated in animals treated with CP-673451. The results indicate that perturbed PDGF-BB/PDGFRp signaling and pericyte accumulation in the airway wall may contribute to airway remodeling in chronic allergic asthma.
机译：肌纤维细胞积累，龈上纤维化和血管重塑是一种复杂的慢性哮喘的特征，但机制尚不清楚。血小板衍生的生长因子（PDGFS）调节各种间充质细胞的命运和功能，并涉及肺纤维化的介质。然而，尚不清楚通过PDGFRP进行PDGF-BB信号传导，这对于血管募集血管至关重要，对慢性哮喘的气道重塑起作用。在本研究中，我们使用了选择性PDGFR（CP-673451）来研究PDGFRP信号传导在Airway重塑和肺功能障碍中的作用，在建立的房屋粉尘诱导的慢性过敏性哮喘的慢性过敏性哮喘患者中。出乎意料，我们发现PDGFR3信号传导的药理抑制在慢性气动理曝光的背景下导致加剧肺功能障碍和气道平滑肌增厚。进一步的研究表明，对小鼠的气动原挑战症的炎症反应与降低的PDGF-BB表达有关和损失有关来自气道微血管系统的截瘫。并行，在慢性发炎的气道的亚斯皮目中积累的细胞阳性细胞阳性。用CP-673451处理的动物加剧了该方法。结果表明扰动PDGF-BB / PDGFRP信号和周刊气道墙中的积累可能有助于慢性逆变的气道重塑C哮喘。

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