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内皮细胞衍生的外泌体通过激活PI3K/Akt/Bcl-2信号通路抑制成骨细胞凋亡和类固醇诱导的股骨头坏死进展。

Endothelial Cell-Derived Exosomes Inhibit Osteoblast Apoptosis and Steroid-Induced Necrosis of Femoral Head Progression by Activating the PI3K/Akt/Bcl-2 Pathway.

作者信息

Sun Jie, Yao Chen, Luo Wanxin, Ge Xingyu, Zheng Wenjie, Sun Chi, Zhang Yafeng

机构信息

Department of Orthopaedics, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.

Research Centre of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.

出版信息

J Tissue Eng Regen Med. 2024 May 10;2024:3870988. doi: 10.1155/2024/3870988. eCollection 2024.

DOI:10.1155/2024/3870988
PMID:40225754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11918886/
Abstract

The aim of the study was to investigate the therapeutic potential of exosomes secreted by endothelial cells (EC-exos) on steroid-induced osteonecrosis of femoral head (SNFH). First, we successfully obtained EC-exos through differential centrifugation. Then, the effects of EC-exos on mouse embryo osteoblast precursor (MC3T3-E1) cells under high concentration of dexamethasone (Dex) were analysed , which included cell migration, viability, and apoptosis. , a SNFH rat model was successfully established and treated with EC-exos. Micro-computed tomography (micro-CT) and haematoxylin and eosin (H&E) were used to observe femoral trabeculae. Our results showed that EC-exos improved cell viability and migration of osteoblasts and reduced the apoptotic effect of high concentration of Dex on osteoblasts . Phosphoinositide 3-kinase (PI3K)/Akt/Bcl-2 signalling pathway was activated in MC3T3-E1 cells under the response to EC-exos. , increased bone volume per tissue volume (BV/TV) (=0.031), trabecular thickness (Tb.Th) (=0.020), and decreased separation (Tb.Sp) (=0.040) were observed in SNFH rats treated with EC-exos. H&E staining revealed fewer empty lacunae and pyknotic osteocytes in trabeculae. The expression of Bcl-2 and Akt in EC-exos group was significantly increased in trabeculae tissue. Overall, our finding indicated that EC-exos could attenuate SNFH by inhibiting osteoblast apoptosis via the PI3K/Akt/Bcl-2 pathway.

摘要

本研究的目的是探讨内皮细胞分泌的外泌体（EC-外泌体）对类固醇诱导的股骨头坏死（SNFH）的治疗潜力。首先，我们通过差速离心成功获得了EC-外泌体。然后，分析了EC-外泌体对高浓度地塞米松（Dex）作用下的小鼠胚胎成骨细胞前体（MC3T3-E1）细胞的影响，包括细胞迁移、活力和凋亡。接着，成功建立了SNFH大鼠模型并用EC-外泌体进行治疗。使用微型计算机断层扫描（micro-CT）和苏木精-伊红（H&E）染色观察股骨小梁。我们的结果表明，EC-外泌体提高了成骨细胞的活力和迁移能力，并降低了高浓度Dex对成骨细胞的凋亡作用。在对EC-外泌体的反应中，MC3T3-E1细胞中的磷酸肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/B细胞淋巴瘤-2（Bcl-2）信号通路被激活。此外，在用EC-外泌体治疗的SNFH大鼠中，观察到组织体积骨体积（BV/TV）增加（=0.031）、小梁厚度（Tb.Th）增加（=0.020）和骨小梁间距（Tb.Sp）减小（=0.040）。H&E染色显示小梁中空陷窝和固缩骨细胞较少。EC-外泌体组小梁组织中Bcl-2和Akt的表达显著增加。总体而言，我们的研究结果表明，EC-外泌体可通过PI3K/Akt/Bcl-2途径抑制成骨细胞凋亡，从而减轻SNFH。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/1b68950148c9/JTERM2024-3870988.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/b6c6715ee0c8/JTERM2024-3870988.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/198a3b63e78b/JTERM2024-3870988.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/f8b380ddbceb/JTERM2024-3870988.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/0163dab3701c/JTERM2024-3870988.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/7067eedf696e/JTERM2024-3870988.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/1b68950148c9/JTERM2024-3870988.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/b6c6715ee0c8/JTERM2024-3870988.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/198a3b63e78b/JTERM2024-3870988.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/f8b380ddbceb/JTERM2024-3870988.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/0163dab3701c/JTERM2024-3870988.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/7067eedf696e/JTERM2024-3870988.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1521/11918886/1b68950148c9/JTERM2024-3870988.006.jpg

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