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首页> 外文期刊>Aging cell. >Muscle precursor cells isolated from aged rats exhibit an increased tumor necrosis factor- response
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Muscle precursor cells isolated from aged rats exhibit an increased tumor necrosis factor- response

机译：从衰老大鼠中分离出的肌肉前体细胞表现出增加的肿瘤坏死因子反应

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Improving muscle precursor cell (MPC, muscle-specific stem cells) function during aging has been implicated as a key therapeutic target for improving age-related skeletal muscle loss. MPC dysfunction during aging can be attributed to both the aging MPC population and the changing environment in skeletal muscle. Previous reports have identified elevated levels of tumor necrosis factor-α (TNF-α) in aging, both circulating and locally in skeletal muscle. The purpose of the present study was to determine if age-related differences exist between TNF-α-induced nuclear factor-kappa B (NF-κB) activation and expression of apoptotic gene targets. MPCs isolated from 32-month-old animals exhibited an increased NF-κB activation in response to 1, 5, and 20 ng mL ?1 TNF-α, compared to MPCs isolated from 3-month-old animals. No age differences were observed in the rapid canonical signaling events leading to NF-κB activation or in the increase in mRNA levels for TNF receptor 1, TNF receptor 2, TNF receptor-associated factor 2 (TRAF2), or Fas (CD95) observed after 2 h of TNF-α stimulation. Interestingly, mRNA levels for TRAF2 and the cell death-inducing receptor, Fas (CD95), were persistently upregulated in response to 24 h TNF-α treatment in MPCs isolated from 32-month-old animals, compared to 3-month-old animals. Our data indicate that age-related differences may exist in the regulatory mechanisms responsible for NF-κB inactivation, which may have an effect on TNF-α-induced apoptotic signaling. These findings improve our understanding of the interaction between aged MPCs and the changing environment associated with age, which is critical for the development of potential clinical interventions aimed at improving MPC function with age.
机译：衰老过程中改善肌肉前体细胞（MPC，特定于肌肉的干细胞）的功能已被认为是改善与年龄有关的骨骼肌丢失的关键治疗靶标。 MPC衰老过程中的功能障碍可归因于MPC种群的衰老和骨骼肌环境的变化。以前的报告已经发现，在骨骼肌中循环和局部衰老时，肿瘤坏死因子-α（TNF-α）的水平升高。本研究的目的是确定在TNF-α诱导的核因子-κB（NF-κB）激活与凋亡基因靶标表达之间是否存在年龄相关差异。与从3个月大的动物分离的MPC相比，从32个月大的动物分离的MPC表现出对1、5和20 ng mL ？1 TNF-α的响应，NF-κB活化增加。动物。在导致NF-κB激活的快速经典信号事件或TNF受体1，TNF受体2，TNF受体相关因子2（TRAF2）或Fas（CD95）的mRNA水平增加方面，未观察到年龄差异。 TNF-α刺激2小时。有趣的是，相比于3个月大的动物，从32个月大的动物分离的MPC中，响应24 hTNF-α处理，TRAF2和细胞死亡诱导受体Fas（CD95）的mRNA水平持续上调。 。我们的数据表明，与年龄相关的差异可能在负责NF-κB失活的调节机制中存在，这可能对TNF-α诱导的凋亡信号传导有影响。这些发现提高了我们对老年MPC与年龄相关的不断变化的环境之间相互作用的理解，这对于开发旨在随着年龄的增长改善MPC功能的潜在临床干预措施至关重要。

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