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水凝胶交联一氧化氮程序释放调控人骨髓间充质干细胞的来源依赖性血管生成行为。

Hydrogel cross-linking-programmed release of nitric oxide regulates source-dependent angiogenic behaviors of human mesenchymal stem cell.

机构信息

Department of Medical Engineering, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.

TMD LAB Co., Ltd., Seoul 03722, Republic of Korea.

出版信息

Sci Adv. 2020 Feb 26;6(9):eaay5413. doi: 10.1126/sciadv.aay5413. eCollection 2020 Feb.

DOI:10.1126/sciadv.aay5413
PMID:32133403
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7043909/
Abstract

Angiogenesis is stimulated by nitric oxide (NO) production in endothelial cells (ECs). Although proangiogenic actions of human mesenchymal stem cells (hMSCs) have been extensively studied, the mechanistic role of NO in this action remains obscure. Here, we used a gelatin hydrogel that releases NO upon crosslinking by a transglutaminase reaction ("NO gel"). Then, the source-specific behaviors of bone marrow versus adipose tissue-derived hMSCs (BMSCs versus ADSCs) were monitored in the NO gels. NO inhibition resulted in significant decreases in their angiogenic activities. The NO gel induced pericyte-like characteristics in BMSCs in contrast to EC differentiation in ADSCs, as evidenced by tube stabilization versus tube formation, 3D colocalization versus 2D coformation with EC tube networks, pericyte-like wound healing versus EC-like vasculogenesis in gel plugs, and pericyte versus EC marker production. These results provide previously unidentified insights into the effects of NO in regulating hMSC source-specific angiogenic mechanisms and their therapeutic applications.

摘要

血管生成是由内皮细胞（ECs）中一氧化氮（NO）的产生所刺激的。尽管人类间充质干细胞（hMSCs）的促血管生成作用已被广泛研究，但 NO 在这种作用中的机制作用仍不清楚。在这里，我们使用了一种在通过转谷氨酰胺酶反应交联时释放 NO 的明胶水凝胶（“NO 凝胶”）。然后，在 NO 凝胶中监测骨髓来源与脂肪组织来源的 hMSCs（BMSCs 与 ADSCs）的来源特异性行为。NO 抑制导致它们的血管生成活性显著降低。NO 凝胶诱导 BMSCs 表现出类似于周细胞的特征，而 ADSCs 则分化为 EC，这表现在管稳定与管形成、3D 共定位与 2D 与 EC 管网络的共形成、凝胶塞中的周细胞样伤口愈合与 EC 样血管生成、以及周细胞与 EC 标志物的产生。这些结果提供了对 NO 调节 hMSC 来源特异性血管生成机制及其治疗应用的影响的以前未被识别的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/eebf07d6320e/aay5413-F6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/eebf07d6320e/aay5413-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/faf409b64104/aay5413-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/ce651cc55d61/aay5413-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/89f9ab8e5478/aay5413-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/a2bd85098325/aay5413-F4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a95/7043909/eebf07d6320e/aay5413-F6.jpg

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