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CPT1C 通过调节自噬促进葡萄糖剥夺下人骨髓间充质干细胞的存活。

CPT1C promotes human mesenchymal stem cells survival under glucose deprivation through the modulation of autophagy.

机构信息

Basic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya (UIC), 08195, Sant Cugat del Vallès, Spain.

Regenerative Medicine Institute, Universitat Internacional de Catalunya, 08195, Sant Cugat del Vallès, Spain.

出版信息

Sci Rep. 2018 May 3;8(1):6997. doi: 10.1038/s41598-018-25485-7.

DOI:10.1038/s41598-018-25485-7
PMID:29725060
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5934389/
Abstract

Human mesenchymal stem cells (hMSCs) are widely used in regenerative medicine. In some applications, they must survive under low nutrient conditions engendered by avascularity. Strategies to improve hMSCs survival may be of high relevance in tissue engineering. Carnitine palmitoyltransferase 1 C (CPT1C) is a pseudoenzyme exclusively expressed in neurons and cancer cells. In the present study, we show that CPT1C is also expressed in hMSCs and protects them against glucose starvation, glycolysis inhibition, and oxygen/glucose deprivation. CPT1C overexpression in hMSCs did not increase fatty acid oxidation capacity, indicating that the role of CPT1C in these cells is different from that described in tumor cells. The increased survival of CPT1C-overexpressing hMSCs observed during glucose deficiency was found to be the result of autophagy enhancement, leading to a greater number of lipid droplets and increased intracellular ATP levels. In fact, inhibition of autophagy or lipolysis was observed to completely block the protective effects of CPT1C. Our results indicate that CPT1C-mediated autophagy enhancement in glucose deprivation conditions allows a greater availability of lipids to be used as fuel substrate for ATP generation, revealing a new role of CPT1C in stem cell adaptation to low nutrient environments.

摘要

人骨髓间充质干细胞（hMSCs）广泛用于再生医学。在某些应用中，它们必须在血管生成引起的低营养条件下存活。提高 hMSCs 存活率的策略在组织工程中可能具有重要意义。肉毒碱棕榈酰转移酶 1C（CPT1C）是一种仅在神经元和癌细胞中表达的伪酶。在本研究中，我们表明 CPT1C 也在 hMSCs 中表达，并保护它们免受葡萄糖饥饿、糖酵解抑制和缺氧/葡萄糖剥夺的影响。hMSCs 中 CPT1C 的过表达并没有增加脂肪酸氧化能力，这表明 CPT1C 在这些细胞中的作用与在肿瘤细胞中描述的不同。在葡萄糖缺乏时观察到的 CPT1C 过表达 hMSCs 的存活率增加被发现是自噬增强的结果，导致更多的脂滴和增加的细胞内 ATP 水平。事实上，自噬或脂肪分解的抑制被观察到完全阻断了 CPT1C 的保护作用。我们的结果表明，CPT1C 介导的自噬增强在葡萄糖剥夺条件下允许更多的脂质可用作产生 ATP 的燃料底物，揭示了 CPT1C 在干细胞适应低营养环境中的新作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/1c7b7c28484b/41598_2018_25485_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/b50578a02e92/41598_2018_25485_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/70dceeff26c7/41598_2018_25485_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/b848f12a0da8/41598_2018_25485_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/022798645bc2/41598_2018_25485_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/3796c873a62b/41598_2018_25485_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/7201b3284cff/41598_2018_25485_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/1c7b7c28484b/41598_2018_25485_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/b50578a02e92/41598_2018_25485_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/70dceeff26c7/41598_2018_25485_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/b848f12a0da8/41598_2018_25485_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/022798645bc2/41598_2018_25485_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/3796c873a62b/41598_2018_25485_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/7201b3284cff/41598_2018_25485_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9206/5934389/1c7b7c28484b/41598_2018_25485_Fig7_HTML.jpg

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Carnitine palmitoyltransferase 1C: From cognition to cancer.
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