AGING CELL:缺氧驱动老年人肌腱变性

2019-04-13 海北 MedSci原创

年龄相关的肌腱变性的特征在于表型变化,其中肌腱细胞显示出纤维软骨细胞和矿化纤维软骨细胞的特征。

年龄相关的肌腱变性的特征在于表型变化,其中肌腱细胞显示出纤维软骨细胞和矿化纤维软骨细胞的特征。

由于在肌腱血管分布减少的区域已经注意到肌腱变性,研究人员假设缺氧是肌腱变性表型发展的原因,并且这些影响在老年肌腱细胞中更为明显。

衰老的,肌腱变性的和年轻人的肌腱细胞的缺氧(1%O 2)培养能够导致老年肌腱细胞中的矿化纤维软骨细胞表型,以及年轻和肌腱变性的肌腱细胞中的纤维软骨细胞表型。

对该表型变化负责的分子机制的研究表明,老年肌腱细胞中的纤维软骨细胞表型发生了响应缺氧时Rac1活性降低。然而,在年轻的缺氧肌腱细胞中,纤维软骨细胞表型发生伴随着Rac1活性的降低,以及RhoA活性的增加。

使用药理学和腺病毒操作,研究人员进一步证实这些对肌腱细胞表型的缺氧作用与体外人细胞培养和肌腱外植体中RhoA / Rac1 GTP酶的活性直接相关。

这些结果表明,缺氧驱动肌腱细胞表型变化,并为衰老时发生的人类肌腱病的发展提供分子机制解释。


原始出处:

Rowena McBeath et al. Tendinosis develops from age‐ and oxygen tension‐dependent modulation of Rac1 activity. AGING CELL, 2019; doi:  https://doi.org/10.1111/acel.12934


本文系梅斯医学(MedSci)原创编译整理,转载需授权

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    2019-12-12 维他命
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    2019-04-22 清风拂面

    谢谢分享学习

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    2019-04-15 清风拂面

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    2019-04-15 huangdf
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    2019-04-15 丁鹏鹏