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脂肪间充质干细胞和牙龈间充质干细胞在内皮修复方面具有相似的效果。

Adipose mesenchymal stem cells and gingival mesenchymal stem cells have a comparable effect in endothelium repair.

作者信息

Yang Ke, Xie Dongmei, Lin Wanwen, Xiang Peng, Peng Chaoquan

机构信息

Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.

Key Laboratory for Stem Cells and Tissue Engineering, Center for Stem Cell Biology and Tissue Engineering, Ministry of Education, Sun Yat-sen University, Guangzhou, Guangdong 510600, P.R. China.

出版信息

Exp Ther Med. 2021 Dec;22(6):1415. doi: 10.3892/etm.2021.10851. Epub 2021 Oct 8.

DOI:10.3892/etm.2021.10851
PMID:34676008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8524764/
Abstract

Restenosis is the major factor influencing the long-term success rate of angioplasty and stent implantation and effective strategies to prevent restenosis remain limited. Mesenchymal stem cells (MSCs) are pluripotent stem cells capable of self-renewal and multidirectional differentiation, which may be able to promote endothelium repair, thereby reducing restenosis. The present study aimed to evaluate the effects of adipose MSCs (AMSCs) and gingival MSCs (GMSCs) on endothelium repair. MSCs were isolated from two human tissue types, namely adipose tissue and gingival tissue, and the effects of AMSCs and GMSCs in endothelium repair and on vascular smooth muscle cell (SMC) growth were examined. To compare the feasibility of using AMSCs and GMSCs for the repair of endothelium damage in endothelial cell (EC) damage and vasoproliferative disorders, an model of endothelium repair in a co-culture system was developed. It was indicated that AMSCs and GMSCs expressed characteristic MSC markers (CD105 and CD166). 3H-thymidine incorporation in the co-culture group of AMSCs and SMCs in the presence of ECs was lower compared with that in the GMSC and SMC co-culture group. The protein expression level of proliferating cell nuclear antigen in the co-culture group of AMSCs and SMCs in the presence of ECs were lower compared with that in the GMSC and SMC co-culture group. After co-culture with ECs for 5 days, 25.71±3.08% of AMSCs began to express CD31 protein and 20.06±2.09% of GMSCs began to express CD31 protein. Furthermore, anti-VEGF antibody was able to inhibit MSC differentiation. Collectively, the present results suggested that seeding of AMSCs had a stronger effect to inhibit the proliferation and migration of SMCs compared with GMSCs.

摘要

再狭窄是影响血管成形术和支架植入长期成功率的主要因素,而预防再狭窄的有效策略仍然有限。间充质干细胞(MSCs)是能够自我更新和多向分化的多能干细胞,可能能够促进内皮修复,从而减少再狭窄。本研究旨在评估脂肪间充质干细胞(AMSCs)和牙龈间充质干细胞(GMSCs)对内皮修复的影响。从两种人体组织类型即脂肪组织和牙龈组织中分离出间充质干细胞,并检测了AMSCs和GMSCs在内皮修复及对血管平滑肌细胞(SMC)生长方面的作用。为比较使用AMSCs和GMSCs修复内皮细胞(EC)损伤和血管增殖性疾病中内皮损伤的可行性,建立了共培养系统中的内皮修复模型。结果表明,AMSCs和GMSCs表达特征性的间充质干细胞标志物(CD105和CD166)。与GMSC和SMC共培养组相比,在有ECs存在的情况下,AMSCs和SMC共培养组中3H-胸腺嘧啶核苷掺入量较低。与GMSC和SMC共培养组相比,在有ECs存在的情况下,AMSCs和SMC共培养组中增殖细胞核抗原的蛋白表达水平较低。与ECs共培养5天后,25.71±3.08%的AMSCs开始表达CD31蛋白,20.06±2.09%的GMSCs开始表达CD31蛋白。此外,抗VEGF抗体能够抑制间充质干细胞的分化。总体而言,目前的结果表明,与GMSCs相比,接种AMSCs对抑制SMC的增殖和迁移具有更强的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/dea80f9c2f61/etm-22-06-10851-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/29633d5e2594/etm-22-06-10851-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/579d6c48744d/etm-22-06-10851-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/9e52442e92f5/etm-22-06-10851-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/ea3d70532d02/etm-22-06-10851-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/b100a88cf46a/etm-22-06-10851-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/416e8e3ea154/etm-22-06-10851-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/985206bd4e4c/etm-22-06-10851-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/5ffa5a3d89bd/etm-22-06-10851-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/dea80f9c2f61/etm-22-06-10851-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/29633d5e2594/etm-22-06-10851-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/579d6c48744d/etm-22-06-10851-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/9e52442e92f5/etm-22-06-10851-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/ea3d70532d02/etm-22-06-10851-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/b100a88cf46a/etm-22-06-10851-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/416e8e3ea154/etm-22-06-10851-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/985206bd4e4c/etm-22-06-10851-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/5ffa5a3d89bd/etm-22-06-10851-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b46e/8524764/dea80f9c2f61/etm-22-06-10851-g08.jpg

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