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原头蚴来源的外泌体在体外促进血管生成的作用。

The In Vitro Promoting Angiogenesis Roles of Exosomes Derived from the Protoscoleces of .

机构信息

Department of Pathogen Biology, College of Basic Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.

出版信息

J Microbiol Biotechnol. 2024 Jul 28;34(7):1410-1418. doi: 10.4014/jmb.2403.03042. Epub 2024 May 23.

DOI:10.4014/jmb.2403.03042
PMID:38858095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11294651/
Abstract

Alveolar echinococcosis (AE) is a persistent parasite condition that causes the formation of tumor-like growths. It is a challenge to treat the disease. These growths need neovascularization to get their oxygen and nutrients, and the disease is prolonged and severe. Considerable research has been conducted on exosomes and their interactions with in the context of immunological evasion by the host. However, the extent of their involvement in angiogenesis needs to be conducted. The primary objective of this investigation was to preliminarily explore the effect of exosomes produced from protoscoleces (PSC-exo) on angiogenesis, to elucidate the mechanism of their roles in the regulation of the downstream pathway of VEGFA activation, and to provide ideas for the development of novel treatments for AE. The study evaluated the impact of PSC-exo increases proliferation, migration, invasion, and tube formation of HUVECs at concentrations of up to 50 μg/ml. In addition, the study sought to validate the findings in vivo. This effect involved increased VEGFA expression at gene and protein levels and AKT/mTOR pathway activation. PSC-exo are crucial in promoting angiogenesis through VEGFA upregulation and AKT/mTOR signaling. This research contributes to our knowledge of neovascularization in AE.

摘要

泡型包虫病(AE)是一种持续存在的寄生虫病,会导致肿瘤样生长。治疗这种疾病具有挑战性。这些生长需要新血管生成来获取氧气和营养,疾病会延长和加重。在宿主免疫逃避方面,已经对细胞外囊泡及其与的相互作用进行了大量研究。然而,需要进一步研究它们在血管生成中的参与程度。本研究的主要目的是初步探讨原头节来源的细胞外囊泡(PSC-exo)对血管生成的影响,阐明它们在调节 VEGFA 激活下游途径中的作用机制,并为 AE 的新型治疗方法的开发提供思路。研究评估了 PSC-exo 在高达 50μg/ml 的浓度下增加人脐静脉内皮细胞(HUVEC)增殖、迁移、侵袭和管形成的作用。此外,本研究还试图在体内验证这些发现。这种作用涉及基因和蛋白水平上 VEGFA 表达的增加以及 AKT/mTOR 通路的激活。PSC-exo 通过上调 VEGFA 和 AKT/mTOR 信号通路在促进血管生成中起关键作用。本研究有助于我们了解 AE 中的新血管生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/95c5920c6dcf/jmb-34-7-1410-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/ab88f684c437/jmb-34-7-1410-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/aaa037f3f860/jmb-34-7-1410-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/17cc42615906/jmb-34-7-1410-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/1690e24232bc/jmb-34-7-1410-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/95c5920c6dcf/jmb-34-7-1410-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/ab88f684c437/jmb-34-7-1410-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/aaa037f3f860/jmb-34-7-1410-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/17cc42615906/jmb-34-7-1410-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/1690e24232bc/jmb-34-7-1410-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b13/11294651/95c5920c6dcf/jmb-34-7-1410-f5.jpg

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本文引用的文献

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2
Effects of LAIR-1 on hepatocellular carcinoma cell proliferation and invasion via PI3K-AKT-mTOR pathway regulation.LAIR-1 通过调控 PI3K-AKT-mTOR 通路对肝癌细胞增殖和侵袭的影响。
Immun Inflamm Dis. 2023 Aug;11(8):e982. doi: 10.1002/iid3.982.
3
Extracellular vesicles secreted by Echinococcus multilocularis: important players in angiogenesis promotion.
多房棘球绦虫分泌的细胞外囊泡:促进血管生成的重要参与者。
Microbes Infect. 2023 Sep-Oct;25(7):105147. doi: 10.1016/j.micinf.2023.105147. Epub 2023 May 2.
4
ESM1 promotes angiogenesis in colorectal cancer by activating PI3K/Akt/mTOR pathway, thus accelerating tumor progression.ESM1 通过激活 PI3K/Akt/mTOR 通路促进结直肠癌血管生成,从而加速肿瘤进展。
Aging (Albany NY). 2023 Mar 7;15(8):2920-2936. doi: 10.18632/aging.204559.
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Exosomal circTUBGCP4 promotes vascular endothelial cell tipping and colorectal cancer metastasis by activating Akt signaling pathway.外泌体环状 RNA TUBGCP4 通过激活 Akt 信号通路促进血管内皮细胞突出和结直肠癌细胞转移。
J Exp Clin Cancer Res. 2023 Feb 15;42(1):46. doi: 10.1186/s13046-023-02619-y.
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