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首页> 外文期刊>Physiological Reports >Hydrostatic pressure suppresses fibrotic changes via Akt/GSK‐3 signaling in human cardiac fibroblasts
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Hydrostatic pressure suppresses fibrotic changes via Akt/GSK‐3 signaling in human cardiac fibroblasts

机译：静水压通过人心脏成纤维细胞中的Akt / GSK-3信号传导抑制纤维化变化

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Mechanical stresses play important roles in the process of constructing and modifying heart structure. It has been well established that stretch force acting on cardiac fibroblasts induces fibrosis. However, the effects of compressive force, that is , hydrostatic pressure (HP), have not been well elucidated. We thus evaluated the effects of HP using a pressure‐loading apparatus in human cardiac fibroblasts (HCFs) in?vitro. In this study, high HP (200?mmHg) resulted in significant phosphorylation of Akt in HCFs. HP then greatly inhibited glycogen synthase kinase 3 (GSK‐3) α , which acts downstream of the PI3K/Akt pathway. Similarly, HP suppressed mRNA transcription of inflammatory cytokine‐6, collagen I and III, and matrix metalloproteinase 1, compared with an atmospheric pressure condition. Furthermore, HP inhibited collagen matrix production in a three‐dimensional HCF culture. Taken together, high HP suppressed the differentiation of fibroblasts into the myofibroblast phenotype. HP under certain conditions suppressed cardiac fibrosis via Akt/GSK‐3 signaling in HCFs. These results might help to elucidate the pathology of some types of heart disease.
机译：机械应力在心脏结构的构建和修改过程中起着重要作用。众所周知，作用在心脏成纤维细胞上的拉伸力会引起纤维化。但是，尚未充分阐明压缩力的影响，即静水压力（HP）。因此，我们使用压力加载设备评估了HP对体外人心脏成纤维细胞（HCF）的影响。在这项研究中，高HP（200？mmHg）导致HCF中Akt的显着磷酸化。然后，HP大大抑制了糖原合酶激酶3（GSK-3）α，它在PI3K / Akt途径的下游起作用。同样，与大气压条件相比，HP抑制了炎性细胞因子-6，I型和III型胶原以及基质金属蛋白酶1的mRNA转录。此外，HP还抑制了三维HCF培养物中胶原基质的产生。两者合计，高HP抑制成纤维细胞分化为成肌纤维细胞表型。 HP在某些情况下会通过HCF中的Akt / GSK-3信号抑制心脏纤维化。这些结果可能有助于阐明某些类型的心脏病的病理。

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