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Nesfatin-1通过mTOR途径促进大鼠肌腱来源干细胞的成骨分化及肌腱异位骨化的发病机制。

Nesfatin-1 Promotes the Osteogenic Differentiation of Tendon-Derived Stem Cells and the Pathogenesis of Heterotopic Ossification in Rat Tendons via the mTOR Pathway.

作者信息

Xu Kai, Zhang Zhanfeng, Chen Mengyao, Moqbel Safwat Adel Abdo, He Yuzhe, Ma Chiyuan, Jiang Lifeng, Xiong Yan, Wu Lidong

机构信息

Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Department of Orthopedic Surgery, The First People's Hospital of Huzhou, Huzhou, China.

出版信息

Front Cell Dev Biol. 2020 Dec 3;8:547342. doi: 10.3389/fcell.2020.547342. eCollection 2020.

DOI:10.3389/fcell.2020.547342
PMID:33344440
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7744791/
Abstract

Heterotopic ossification (HO) is a pathological condition involved in tendinopathy. Adipokines are known to play a key role in HO of tendinopathy. Nesfatin-1, an 82-amino acid adipokine is closely reportedly associated with diabetes mellitus (DM), which, in turn, is closely related to tendinopathy. In the present study, we aimed to investigate the effects of nesfatin-1 on the osteogenic differentiation of tendon-derived stem cells (TDSCs) and the pathogenesis of tendinopathy in rats. , TDSCs were incubated in osteogenic induction medium for 14 days with different nesfatin-1 concentration. , Sprague Dawley rats underwent Achilles tenotomy to evaluate the effect of nesfatin-1 on tendinopathy. Our results showed that the expression of nesfatin-1 expression in tendinopathy patients was significantly higher than that in healthy subjects. Nesfatin-1 affected the cytoskeleton and reduced the migration ability of TDSCs . Furthermore, nesfatin-1 inhibited the expression of , , and and promoted the expression of osteogenic genes, such as , , and RUNX2; these results suggested that nesfatin-1 inhibits cell migration, adversely impacts tendon phenotype, promotes osteogenic differentiation of TDSCs and the pathogenesis of HO in rat tendons. Moreover, we observed that nesfatin-1 suppressed autophagy and activated the mammalian target of rapamycin (mTOR) pathway both and . The suppression of the mTOR pathway alleviated nesfatin-1-induced HO development in rat tendons. Thus, nesfatin-1 promotes the osteogenic differentiation of TDSC and the pathogenesis of HO in rat tendons via the mTOR pathway; these findings highlight a new potential therapeutic target for tendinopathy.

摘要

异位骨化（HO）是一种与肌腱病相关的病理状况。已知脂肪因子在肌腱病的异位骨化中起关键作用。Nesfatin-1是一种由82个氨基酸组成的脂肪因子，据报道与糖尿病（DM）密切相关，而糖尿病又与肌腱病密切相关。在本研究中，我们旨在研究Nesfatin-1对肌腱衍生干细胞（TDSCs）成骨分化的影响以及大鼠肌腱病的发病机制。将TDSCs在不同浓度的Nesfatin-1的成骨诱导培养基中培养14天。对Sprague Dawley大鼠进行跟腱切断术，以评估Nesfatin-1对肌腱病的影响。我们的结果表明，肌腱病患者中Nesfatin-1的表达明显高于健康受试者。Nesfatin-1影响细胞骨架并降低TDSCs的迁移能力。此外，Nesfatin-1抑制、和的表达，并促进成骨基因如、和RUNX2的表达；这些结果表明，Nesfatin-1抑制细胞迁移，对肌腱表型产生不利影响，促进TDSCs的成骨分化以及大鼠肌腱中HO的发病机制。此外，我们观察到Nesfatin-1在体内和体外均抑制自噬并激活雷帕霉素哺乳动物靶标（mTOR）途径。mTOR途径的抑制减轻了Nesfatin-1诱导的大鼠肌腱中HO的发展。因此，Nesfatin-1通过mTOR途径促进TDSC的成骨分化以及大鼠肌腱中HO的发病机制；这些发现突出了肌腱病一个新的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f2/7744791/b9ffb113ec1d/fcell-08-547342-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f2/7744791/b9ffb113ec1d/fcell-08-547342-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f2/7744791/142dafd5794e/fcell-08-547342-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f2/7744791/19baea634cb3/fcell-08-547342-g005.jpg
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