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IL-10 通过调节 ERK 和 STAT3 的活性来调节成体神经发生。

IL-10 regulates adult neurogenesis by modulating ERK and STAT3 activity.

机构信息

Unit of Brain Ischemia, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona Spain ; Department of Brain Ischemia and Neurodegeneration, Institute of Biomedical Research of Barcelona, Consejo Superior de Investigaciones Científicas, Barcelona Spain.

Laboratory for Neurobiology and Gene Therapy, Faculty of Medicine, KU Leuven, Leuven Belgium ; Leuven Viral Vector Core, KU Leuven, Leuven Belgium.

出版信息

Front Cell Neurosci. 2015 Feb 25;9:57. doi: 10.3389/fncel.2015.00057. eCollection 2015.

DOI:10.3389/fncel.2015.00057
PMID:25762897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4340210/
Abstract

The adult subventricular zone (SVZ) contains Nestin+ progenitors that differentiate mainly into neuroblasts. Our previous data showed that interleukin-10 (IL-10) regulates SVZ adult neurogenesis by up-regulating the expression of pro-neural genes and modulating cell cycle exit. Here we addressed the specific mechanism through which IL-10 carries out its signaling on SVZ progenitors. We found that, in vitro and in vivo, IL-10 targets Nestin+ progenitors and activates the phosphorylation of ERK and STAT3. The action of IL-10 on Nestin+ progenitors is reversed by treatment with a MEK/ERK inhibitor, thus restoring neurogenesis to normal levels. Silencing STAT3 expression by lentiviral vectors also impaired neurogenesis by blocking the effects of IL-10. Our findings unveil ERK and STAT3 as effectors of IL-10 in adult SVZ neurogenesis.

摘要

成年侧脑室下区（SVZ）含有巢蛋白阳性祖细胞，这些祖细胞主要分化为神经母细胞。我们之前的数据表明，白细胞介素 10（IL-10）通过上调神经前体细胞基因的表达并调节细胞周期退出来调节 SVZ 成体神经发生。在这里，我们研究了 IL-10 对 SVZ 祖细胞进行信号传递的具体机制。我们发现，在体外和体内，IL-10 以巢蛋白阳性祖细胞为靶点，并激活 ERK 和 STAT3 的磷酸化。用 MEK/ERK 抑制剂处理可逆转 IL-10 对 Nestin+祖细胞的作用，从而将神经发生恢复到正常水平。通过慢病毒载体沉默 STAT3 表达也会通过阻断 IL-10 的作用而损害神经发生。我们的研究结果揭示了 ERK 和 STAT3 是 IL-10 在成年 SVZ 神经发生中的效应物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/0e808beb19ae/fncel-09-00057-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/147453f4c810/fncel-09-00057-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/1886e5e9d255/fncel-09-00057-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/1be92dbabd59/fncel-09-00057-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/61024ba321eb/fncel-09-00057-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/dc82500e6b4d/fncel-09-00057-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/85cf22093d3a/fncel-09-00057-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/0e808beb19ae/fncel-09-00057-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/147453f4c810/fncel-09-00057-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/1886e5e9d255/fncel-09-00057-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/1be92dbabd59/fncel-09-00057-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/61024ba321eb/fncel-09-00057-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/dc82500e6b4d/fncel-09-00057-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/85cf22093d3a/fncel-09-00057-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7046/4340210/0e808beb19ae/fncel-09-00057-g007.jpg

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