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FAK-p38 signaling serves as a potential target for reverting matrix stiffness-modulated liver sinusoidal endothelial cell defenestration

文献类型：期刊论文

作者Zhang, Xiaoyu3,4,5; Li, Peiwen4,5; Zhou, Jin4,5; Zhang, Ziliang2,4,5; Wu, Huan4,5; Shu, Xinyu3,4,5; Li, Wang3,4,5; Wu, Yi3,4,5; Du, Yu4,5; Lu, Dongyuan3,4,5
刊名BIOMATERIALS
出版日期2024-03-01
卷号305页码:17
ISSN号0142-9612
关键词Liver sinusoidal endothelial cells Fenestrae Liver fibrosis Cytoskeleton remodeling FAK MAPK
DOI10.1016/j.biomaterials.2023.122462
通讯作者Li, Ning(lining_1@imech.ac.cn) ; Long, Mian(mlong@imech.ac.cn)
英文摘要Liver sinusoidal endothelial cells (LSECs) are highly specific endothelial cells which play an essential role in the maintenance of liver homeostasis. During the progression of liver fibrosis, matrix stiffening promotes LSEC defenestration, however, the underlying mechanotransduction mechanism remains poorly understood. Here, we applied stiffness-tunable hydrogels to assess the matrix stiffening-induced phenotypic changes in primary mouse LSECs. Results indicated that increased stiffness promoted LSEC defenestration through cytoskeletal reorganization. LSECs sensed the increased matrix stiffness via focal adhesion kinase (FAK), leading to the activation of p38-mitogen activated protein kinase activated protein kinase 2 (MK2) pathway, thereby inducing actin remodeling via LIM Kinase 1 (LIMK1) and Cofilin. Interestingly, inhibition of FAK or p38-MK2 pathway was able to effectively restore the fenestrae to a certain degree in LSECs isolated from early to late stages of liver fibrosis mice. Thus, this study highlights the impact of mechanotransduction in LSEC defenestration, and provides novel insights for potential therapeutic interventions for liver fibrosis.
WOS关键词FENESTRAE ; ACTIVATION ; CYTOSKELETON ; FIBROSIS ; SIEVE
资助项目National Natural Science Foundation of China[32130061] ; National Natural Science Foundation of China[T2394512] ; National Natural Science Foundation of China[32271366] ; National Key R & D Program of China[2021YFA0719302] ; China Manned Space Flight Technology Project Chinese Space Station Experiment Project[YYWT0901EXP0701] ; Scientific Instrument Developing Project of Chinese Academy of Sci-ences[GJJSTU20220002]
WOS研究方向Engineering ; Materials Science
语种英语
WOS记录号WOS:001165474400001
资助机构National Natural Science Foundation of China ; National Key R & D Program of China ; China Manned Space Flight Technology Project Chinese Space Station Experiment Project ; Scientific Instrument Developing Project of Chinese Academy of Sci-ences
源URL[http://dspace.imech.ac.cn/handle/311007/94507]  
专题力学研究所_国家微重力实验室
通讯作者Li, Ning; Long, Mian
作者单位1.Inst Mech, Chinese Acad Sci, Beijing 100190, Peoples R China
2.Shandong First Med Univ & Shandong Acad Med Sci, Med Sci & Technol Innovat Ctr, Jinan 250117, Peoples R China
3.Univ Chinese Acad Sci, Sch Engn Sci, Beijing 100049, Peoples R China
4.Chinese Acad Sci, Inst Mech, Key Lab Micrograv, Natl Micrograv Lab, Beijing 100190, Peoples R China
5.Chinese Acad Sci, Ctr Biomech & Bioengn, Beijing Key Lab Engn Construct & Mechanobiol, Natl Micrograv Lab,Inst Mech, Beijing 100190, Peoples R China
推荐引用方式
GB/T 7714		 Zhang, Xiaoyu,Li, Peiwen,Zhou, Jin,et al. FAK-p38 signaling serves as a potential target for reverting matrix stiffness-modulated liver sinusoidal endothelial cell defenestration[J]. BIOMATERIALS,2024,305:17.
APA Zhang, Xiaoyu.,Li, Peiwen.,Zhou, Jin.,Zhang, Ziliang.,Wu, Huan.,...&李旺.(2024).FAK-p38 signaling serves as a potential target for reverting matrix stiffness-modulated liver sinusoidal endothelial cell defenestration.BIOMATERIALS,305,17.
MLA Zhang, Xiaoyu,et al."FAK-p38 signaling serves as a potential target for reverting matrix stiffness-modulated liver sinusoidal endothelial cell defenestration".BIOMATERIALS 305(2024):17.

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来源：力学研究所

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