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工程化干细胞通过过表达 SDF-1 改善骨盆神经损伤大鼠模型的神经源性膀胱。

Engineered Stem Cells Improve Neurogenic Bladder by Overexpressing SDF-1 in a Pelvic Nerve Injury Rat Model.

机构信息

Department of Urology, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.

Catholic Integrative Medicine Research Institute, The Catholic University of Korea, Seoul, Republic of Korea.

出版信息

Cell Transplant. 2020 Jan-Dec;29:963689720902466. doi: 10.1177/0963689720902466.

DOI:10.1177/0963689720902466
PMID:32067480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7444235/
Abstract

There is still a lack of sufficient research on the mechanism behind neurogenic bladder (NB) treatment. The aim of this study was to explore the effect of overexpressed stromal cell-derived factor-1 (SDF-1) secreted by engineered immortalized mesenchymal stem cells (imMSCs) on the NB. In this study, primary bone marrow mesenchymal stem cells (BM-MSCs) were transfected into immortalized upregulated SDF-1-engineered BM-MSCs (imMSCs/eSDF-1) or immortalized normal SDF-1-engineered BM-MSCs (imMSCs/eSDF-1). NB rats induced by bilateral pelvic nerve (PN) transection were treated with imMSCs/eSDF-1, imMSCs/eSDF-1, or sham. After a 4-week treatment, the bladder function was assessed by cystometry and voiding pattern analysis. The PN and bladder tissues were evaluated via immunostaining and western blotting analysis. We found that imMSCs/eSDF-1 expressed higher levels of SDF-1 in vitro and in vivo. The treatment of imMSCs/eSDF-1 improved NB and evidently stimulated the recovery of bladder wall in NB rats. The recovery of injured nerve was more effective in the NB+imMSCs/eSDF-1 group than in other groups. High SDF-1 expression improved the levels of vascular endothelial growth factor and basic fibroblast growth factor. Apoptosis was decreased after imMSCs injection, and was detected rarely in the NB+imMSCs/eSDF-1 group. Injection of imMSCs boosted the expression of neuronal nitric oxide synthase, p-AKT, and p-ERK in the NB+imMSCs/eSDF-1 group than in other groups. Our findings demonstrated that overexpression of SDF-1 induced additional MSC homing to the injured tissue, which improved the NB by accelerating the restoration of injured nerve in a rat model.

摘要

目前针对神经原性膀胱（NB）治疗的机制研究仍显不足。本研究旨在探索过表达基质细胞衍生因子-1（SDF-1）对 NB 的影响。本研究中，原代骨髓间充质干细胞（BM-MSCs）转染入永生化过表达 SDF-1 的 BM-MSCs（imMSCs/eSDF-1）或永生化正常 SDF-1 的 BM-MSCs（imMSCs/eSDF-1）。将双侧盆神经（PN）横断诱导的 NB 大鼠分别用 imMSCs/eSDF-1、imMSCs/eSDF-1 或 sham 处理。4 周治疗后，通过膀胱测压和排尿模式分析评估膀胱功能。通过免疫组化和 Western blot 分析评估 PN 和膀胱组织。我们发现 imMSCs/eSDF-1 在体外和体内均表达更高水平的 SDF-1。imMSCs/eSDF-1 治疗改善了 NB，并明显刺激了 NB 大鼠膀胱壁的恢复。NB+imMSCs/eSDF-1 组神经损伤的恢复比其他组更有效。高 SDF-1 表达提高了血管内皮生长因子和碱性成纤维细胞生长因子的水平。注射 imMSCs 后，细胞凋亡减少，在 NB+imMSCs/eSDF-1 组中很少检测到。注射 imMSCs 增加了 NB+imMSCs/eSDF-1 组神经元型一氧化氮合酶、p-AKT 和 p-ERK 的表达。我们的研究结果表明，SDF-1 的过表达诱导更多 MSC 归巢至损伤组织，通过加速损伤神经的恢复，改善了 NB。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/8c130f517d8b/10.1177_0963689720902466-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/e918986add3b/10.1177_0963689720902466-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/ac9483d40efd/10.1177_0963689720902466-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/73b4d88a5f4b/10.1177_0963689720902466-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/d760c9b03224/10.1177_0963689720902466-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/858824df0d96/10.1177_0963689720902466-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/3120caf556dd/10.1177_0963689720902466-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/8c130f517d8b/10.1177_0963689720902466-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/e918986add3b/10.1177_0963689720902466-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/ac9483d40efd/10.1177_0963689720902466-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/73b4d88a5f4b/10.1177_0963689720902466-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/d760c9b03224/10.1177_0963689720902466-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/858824df0d96/10.1177_0963689720902466-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/3120caf556dd/10.1177_0963689720902466-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c25/7444235/8c130f517d8b/10.1177_0963689720902466-fig7.jpg

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