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白细胞介素-11 通过 STAT3 信号通路调节脂肪间充质干细胞的命运。

Interleukin-11 regulates the fate of adipose-derived mesenchymal stem cells via STAT3 signalling pathways.

机构信息

Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.

Shanghai Institute of Cardiovascular Diseases, Shanghai Cardiovascular Medical Center, Institute of Pan-vascular Medicine, Fudan University, Shanghai, China.

出版信息

Cell Prolif. 2020 May;53(5):e12771. doi: 10.1111/cpr.12771. Epub 2020 Apr 9.

DOI:10.1111/cpr.12771
PMID:32270546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7260062/
Abstract

OBJECTIVE

Adipose-derived mesenchymal stem cells (ADSCs) offer great promise as cell therapy for ischaemic diseases. Due to their poor survival in the ischaemic environment, the therapeutic efficacy of ADSCs is still relatively low. Interleukin-11 (IL-11) has been shown to play a key role in promoting cell proliferation and protecting cells from oxidative stress injury. The aim of this study was to determine whether IL-11 could improve therapeutic efficacy of ADSCs in ischaemic diseases.

METHODS AND RESULTS

ADSCs were prepared from inguinal subcutaneous adipose tissue and exposed to hypoxic environment. The protein expression of IL-11 was decreased after hypoxic treatment. In addition, ADSCs viability was increased after IL-11 treatment under hypoxia. Moreover, IL-11 enhanced ADSCs viability in a dose-dependent manner under normoxia. Importantly, IL-11 promoted ADSCs proliferation and migration and protected ADSCs against hydrogen peroxide-induced cellular death. Notably, IL-11 enhanced ADSCs proliferation and migration, also promoted cell survival and apoptosis resistance by STAT3 signalling. In vivo, mice were subjected to limb ischaemia and treated with IL-11 overexpression ADSCs and control ADSCs. IL-11 overexpression ADSCs improved perfusion recovery in the ischaemic muscles.

CONCLUSIONS

We provide the evidence that IL-11 promoted ADSCs proliferation, stimulated ADSCs migration and attenuated ADSCs apoptosis by activation of STAT3 signalling. These results suggest that IL-11 facilitated ADSCs engraftment in ischaemic tissue, thereby enhanced ADSCs therapeutic efficacy.

摘要

目的

脂肪间充质干细胞（ADSCs）作为缺血性疾病的细胞治疗具有很大的应用前景。由于其在缺血环境中的生存能力较差，ADSCs 的治疗效果仍然相对较低。白细胞介素-11（IL-11）已被证明在促进细胞增殖和保护细胞免受氧化应激损伤方面发挥关键作用。本研究旨在确定 IL-11 是否能提高 ADSCs 在缺血性疾病中的治疗效果。

方法和结果

从腹股沟皮下脂肪组织中分离 ADSCs 并暴露于低氧环境中。缺氧处理后，IL-11 的蛋白表达减少。此外，在低氧条件下，IL-11 处理后 ADSCs 的活力增加。此外，IL-11 在常氧条件下以剂量依赖的方式增强 ADSCs 的活力。重要的是，IL-11 促进 ADSCs 的增殖和迁移，并保护 ADSCs 免受过氧化氢诱导的细胞死亡。值得注意的是，IL-11 通过 STAT3 信号通路增强 ADSCs 的增殖和迁移，同时促进细胞存活和抗凋亡。在体内，小鼠肢体缺血后用过表达 IL-11 的 ADSCs 和对照 ADSCs 进行治疗。过表达 IL-11 的 ADSCs 改善了缺血肌肉的灌注恢复。

结论

我们提供的证据表明，IL-11 通过激活 STAT3 信号通路促进 ADSCs 的增殖、刺激 ADSCs 的迁移并减轻 ADSCs 的凋亡。这些结果表明，IL-11 促进 ADSCs 向缺血组织的植入，从而增强 ADSCs 的治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/6c64c62e856c/CPR-53-e12771-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/a022403144ba/CPR-53-e12771-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/94916f7e8da0/CPR-53-e12771-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/7d0bb5f0a3d6/CPR-53-e12771-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/0f208133b505/CPR-53-e12771-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/49794eccf772/CPR-53-e12771-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/6c64c62e856c/CPR-53-e12771-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/a022403144ba/CPR-53-e12771-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/94916f7e8da0/CPR-53-e12771-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/7d0bb5f0a3d6/CPR-53-e12771-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/0f208133b505/CPR-53-e12771-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/49794eccf772/CPR-53-e12771-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ac8/7260062/6c64c62e856c/CPR-53-e12771-g006.jpg

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