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α7 型烟碱型乙酰胆碱受体对大鼠脂肪来源干细胞增殖和迁移的影响。

Effects mediated by the α7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells.

机构信息

Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome.

Department of Pharmaceutical Sciences, Medicinal Chemistry Section "Pietro Pratesi", University of Milan.

出版信息

Eur J Histochem. 2020 Oct 30;64(s2):3159. doi: 10.4081/ejh.2020.3159.

DOI:10.4081/ejh.2020.3159
PMID:33334089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7643034/
Abstract

Adipose-derived stem cells (ASCs) are an attractive source for regenerative medicine as they can be easily isolated, rapidly expandable in culture and show excellent in vitro differentiation potential. Acetylcholine (ACh), one of the main neurotransmitters in central and peripheral nervous systems, plays key roles in the control of several physiological processes also in non-neural tissues. As demonstrated in our previous studies, ACh can contribute to the rat ASCs physiology, negatively modulating ASCs proliferation and migration via M2 muscarinic receptor (mAChR) activation. In the present work we show that rat ASCs also express α7 nicotinic receptors (nAChRs). In particular, we have investigated the effects mediated by the selective activation of α7 nAChRs, which causes a reduction of ASC proliferation without affecting cell survival and morphology, and significantly promotes cell migration via upregulation of the CXCR4 expression. Interestingly, the activation of the α7 nAChR also upregulates the expression of M2 mAChR protein, indicating a cooperation between muscarinic and nicotinic receptors in the inhibition of ASC proliferation.

摘要

脂肪干细胞(ASCs)是再生医学的理想来源,因为它们可以很容易地分离、在培养中快速扩增,并显示出优异的体外分化潜力。乙酰胆碱(ACh)是中枢和外周神经系统中的主要神经递质之一,在控制多种生理过程中发挥着关键作用,也在非神经组织中发挥作用。正如我们之前的研究所示,ACh 可以通过 M2 毒蕈碱受体(mAChR)的激活来调节大鼠 ASCs 的生理机能,从而负调控 ASCs 的增殖和迁移。在本研究中,我们发现大鼠 ASCs 也表达α7 型烟碱型乙酰胆碱受体(nAChR)。具体而言,我们研究了选择性激活α7 nAChR 所介导的作用,该受体的激活可减少 ASC 的增殖,而不影响细胞存活和形态,并且通过上调 CXCR4 的表达显著促进细胞迁移。有趣的是,α7 nAChR 的激活还上调了 M2 mAChR 蛋白的表达,表明烟碱型和毒蕈碱型受体在抑制 ASC 增殖方面存在合作。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/fc2b915bd866/ejh-64-s2-3159-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/acc2d4e1ce71/ejh-64-s2-3159-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/6b39344e05f6/ejh-64-s2-3159-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/ba8ed3c81fc4/ejh-64-s2-3159-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/d9488ce43b98/ejh-64-s2-3159-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/fc2b915bd866/ejh-64-s2-3159-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/acc2d4e1ce71/ejh-64-s2-3159-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/6b39344e05f6/ejh-64-s2-3159-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/ba8ed3c81fc4/ejh-64-s2-3159-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/d9488ce43b98/ejh-64-s2-3159-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1e3/7643034/fc2b915bd866/ejh-64-s2-3159-g005.jpg

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