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机械应力诱导的自噬依赖于细胞骨架。

Mechanical stress-induced autophagy is cytoskeleton dependent.

作者信息

Liu Lin, Zheng Wei, Wei Yuhui, Li Qian, Chen Nan, Xia Qinglin, Wang Lihua, Hu Jun, Zhou Xingfei, Sun Yanhong, Li Bin

机构信息

Key Laboratory of Laboratory Medicine, Ministry of Education of China, Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.

Shanghai Institute of Applied Physics, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.

出版信息

Cell Prolif. 2024 Dec;57(12):e13728. doi: 10.1111/cpr.13728. Epub 2024 Aug 18.

DOI:10.1111/cpr.13728
PMID:39155403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11628738/
Abstract

The cytoskeleton is essential for mechanical signal transduction and autophagy. However, few studies have directly demonstrated the contribution of the cytoskeleton to mechanical stress-induced autophagy. We explored the role of the cytoskeleton in response to compressive force-induced autophagy in human cell lines. Inhibition and activation of cytoskeletal polymerization using small chemical molecules revealed that cytoskeletal microfilaments are required for changes in the number of autophagosomes, whereas microtubules play an auxiliary role in mechanical stress-induced autophagy. The intrinsic mechanical properties and special intracellular distribution of microfilaments may account for a large proportion of compression-induced autophagy. Our experimental data support that microfilaments are core components of mechanotransduction signals.

摘要

细胞骨架对于机械信号转导和自噬至关重要。然而,很少有研究直接证明细胞骨架对机械应力诱导的自噬的作用。我们探讨了细胞骨架在人类细胞系中对压缩力诱导的自噬的反应中的作用。使用小分子抑制和激活细胞骨架聚合表明,细胞骨架微丝是自噬体数量变化所必需的,而微管在机械应力诱导的自噬中起辅助作用。微丝的内在机械特性和特殊的细胞内分布可能在很大程度上解释了压缩诱导的自噬。我们的实验数据支持微丝是机械转导信号的核心成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/ed7247ecae24/CPR-57-e13728-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/097564f6ec32/CPR-57-e13728-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/31f11fafcbcc/CPR-57-e13728-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/49b3fe55b8d6/CPR-57-e13728-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/a9641143a545/CPR-57-e13728-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/ed7247ecae24/CPR-57-e13728-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/097564f6ec32/CPR-57-e13728-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/31f11fafcbcc/CPR-57-e13728-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/49b3fe55b8d6/CPR-57-e13728-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/a9641143a545/CPR-57-e13728-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3717/11628738/ed7247ecae24/CPR-57-e13728-g002.jpg

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