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微小 RNA-9 修饰的骨髓间充质干细胞（BMSCs）通过诱导大鼠血管生成修复重症急性胰腺炎（SAP）。

MicroRNA-9 modified bone marrow-derived mesenchymal stem cells (BMSCs) repair severe acute pancreatitis (SAP) via inducing angiogenesis in rats.

机构信息

Department of General Surgery, Yijishan Hospital, Wannan Medical College, Wuhu, 241001, Anhui, China.

Department of General Surgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang Road, Shanghai, 200072, China.

出版信息

Stem Cell Res Ther. 2018 Oct 25;9(1):282. doi: 10.1186/s13287-018-1022-y.

DOI:10.1186/s13287-018-1022-y
PMID:30359310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6202805/
Abstract

BACKGROUND

Severe acute pancreatitis (SAP) is an acute abdominal disease characterized by pancreatic necrosis and systemic disease. In a previous study, we showed that bone marrow-derived mesenchymal stem cells (BMSCs) can reduce SAP by secreting microRNA (miR)-9; however, the underlying mechanism remains unclear. The present study investigated the mechanism underlying BMSC-induced pancreatic regeneration.

METHODS

BMSCs were isolated, and miR-9 modified/antagonized BMSCs (pri-miR-9-BMSCs/TuD-BMSCs) were generated and injected into SAP rats. The levels of inflammatory cytokines and histopathologic changes were examined using ELISA and H&E staining. Angiogenesis was analyzed by qRT-PCR, western blotting, and immunohistochemistry. Cell function tests, dual luciferase reporter assays, cell co-culture, western blotting, and cell tracing were used to explore the mechanisms underlying miR-9 induced angiogenesis.

RESULTS

Pri-miR-9-BMSCs induced angiogenesis in SAP rats (Ang-1↑, TIE-2↑, and CD31↑) and repaired damaged vascular endothelial cells (VECs) in vitro, promoting angiogenesis (Ang-1↑, TIE-2↑, PI3K↑, AKT↑, p-AKT↑, CD31↑, and CD34↑). Pri-miR-9-BMSCs released miR-9 into VECs or injured pancreatic tissue, targeting the VE-cadherin gene and promoting PI3K/AKT signaling to treat SAP (VE-cadherin↓, β-catenin↓, PI3K↑, p-AKT↑), whereas antagonizing miR-9 in BMSCs did not alleviate or aggravated SAP.

CONCLUSIONS

Pri-miR-9-BMSCs can repair injured pancreatic tissue by secreting miR-9 and promoting angiogenesis.

摘要

背景

重症急性胰腺炎（SAP）是一种以胰腺坏死和全身疾病为特征的急性腹部疾病。在之前的研究中，我们发现骨髓间充质干细胞（BMSCs）可以通过分泌 microRNA（miR）-9 来减轻 SAP；然而，其潜在机制尚不清楚。本研究旨在探讨 BMSC 诱导胰腺再生的机制。

方法

分离 BMSCs，构建并转染前体 miR-9 的 BMSCs（pri-miR-9-BMSCs/TuD-BMSCs），将其注射到 SAP 大鼠体内。通过 ELISA 和 H&E 染色检测炎症因子水平和组织病理学变化。通过 qRT-PCR、western blot 和免疫组化分析血管生成情况。采用细胞功能试验、双荧光素酶报告基因检测、细胞共培养、western blot 和细胞示踪等方法探讨 miR-9 诱导血管生成的机制。

结果

Pri-miR-9-BMSCs 诱导 SAP 大鼠的血管生成（Ang-1↑，TIE-2↑，CD31↑），并在体外修复受损的血管内皮细胞（VECs），促进血管生成（Ang-1↑，TIE-2↑，PI3K↑，AKT↑，p-AKT↑，CD31↑和 CD34↑）。Pri-miR-9-BMSCs 将 miR-9 释放到 VECs 或受损的胰腺组织中，靶向 VE-钙黏蛋白基因，通过激活 PI3K/AKT 信号通路治疗 SAP（VE-钙黏蛋白↓，β-catenin↓，PI3K↑，p-AKT↑），而拮抗 BMSCs 中的 miR-9 既不能缓解也不能加重 SAP。

结论

Pri-miR-9-BMSCs 可通过分泌 miR-9 促进血管生成来修复受损的胰腺组织。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/ba030faaedcb/13287_2018_1022_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/45f56f1bb174/13287_2018_1022_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/b7f06b47b577/13287_2018_1022_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/102c89482f52/13287_2018_1022_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/c0a13b3d6e49/13287_2018_1022_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/ba030faaedcb/13287_2018_1022_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/45f56f1bb174/13287_2018_1022_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/b7f06b47b577/13287_2018_1022_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/102c89482f52/13287_2018_1022_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/42707960215c/13287_2018_1022_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/c0a13b3d6e49/13287_2018_1022_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac0/6202805/ba030faaedcb/13287_2018_1022_Fig6_HTML.jpg

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