期刊
RESPIRATORY RESEARCH
卷 23, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12931-022-02203-6
关键词
COPD systemic environment; Muscle precursor cells; Myogenic capacity; Gene expression
资金
- Spanish Society of Pulmenology and Thoracic Surgery [S 761 1, P10: -12]
- General itat de Catalunya [5G.,03]
- Catalan Pneumology Foundation (FUCAP)
This study investigated the effects of the vascular systemic environment from stable and exacerbated COPD patients on the myogenic behavior of human muscle precursor cells (MPC) in vitro. The findings suggest that the vascular systemic environment during an acute exacerbation has a mitotic effect on MPCs without altering myogenic differentiation outcome. However, after Methylprednisolone treatment of acute exacerbated COPD patients, this mitotic effect is further amplified, but it is followed by a deficient differentiation capacity.
Background: Loss of muscle mass and function are well-recognized systemic manifestations of chronic obstructive pulmonary disease (COPD). Acute exacerbations, in turn, significantly contribute to upgrade these systemic comorbidities. Involvement of myogenic precursors in muscle mass maintenance and recovery is poorly understood. The aim of the present study was to investigate the effects of the vascular systemic environment from stable and exacerbated COPD patients on the myogenic behavior of human muscle precursor cells (MPC) in vitro. Methods: Serum from healthy controls and from stable and exacerbated COPD patients (before and after Methylprednisolone treatment) was used to stimulate human MPC cultures. Proliferation analysis was assessed through BrdU incorporation assays. MPC differentiation was examined through real-time RT-PCR, western blot and immunofluorescence analysis. Results: Stimulation of MPCs with serum obtained from stable COPD patients did not affect myogenic precursor cell function. The vascular systemic environment during an acute exacerbation exerted a mitotic effect on MPCs without altering myogenic differentiation outcome. After Methylprednisolone treatment of acute exacerbated COPD patients, however, the mitotic effect was further amplified, but it was followed by a deficient differentiation capacity. Moreover, these effects were prevented when cells were co-treated with the glucocorticoid receptor antagonist Mifepristone. Conclusion: Our findings suggest that MPC capacity is inherently preserved in COPD patients, but is compromised after systemic administration of MP. This finding strengthens the concept that glucocorticoid treatment over the long term can negatively impact myogenic stem cell fate decisions and interfere with muscle mass recovery.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据