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Wnt7a和Sfrp1在调节小鼠大脑皮质神经祖细胞正常发育中的相反作用

Opposite Roles of Wnt7a and Sfrp1 in Modulating Proper Development of Neural Progenitors in the Mouse Cerebral Cortex.

作者信息

Miao Nan, Bian Shan, Lee Trevor, Mubarak Taufif, Huang Shiying, Wen Zhihong, Hussain Ghulam, Sun Tao

机构信息

Center for Precision Medicine, School of Medicine and School of Biomedical Sciences, Huaqiao University, Xiamen, China.

Department of Cell and Developmental Biology, Weill Cornell Medicine, Cornell University, New York, NY, United States.

出版信息

Front Mol Neurosci. 2018 Jul 17;11:247. doi: 10.3389/fnmol.2018.00247. eCollection 2018.

DOI:10.3389/fnmol.2018.00247
PMID:30065628
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6056652/
Abstract

The Wingless (Wnt)-mediated signals are involved in many important aspects of development of the mammalian cerebral cortex. How Wnts interact with their modulators in cortical development is still unclear. Here, we show that Wnt7a and secreted frizzled-related protein 1 (Sfrp1), a soluble modulator of Wnts, are co-expressed in mouse embryonic cortical neural progenitors (NPs). Knockout of Wnt7a in mice causes microcephaly due to reduced NP population and neurogenesis, and Sfrp1 has an opposing effect compared to Wnt7a. Similar to Dkk1, Sfrp1 decreases the Wnt1 and Wnt7a activity . Our results suggest that Wnt7a and Sfrp1 play opposite roles to ensure proper NP progeny in the developing cortex.

摘要

无翅型（Wnt）介导的信号参与哺乳动物大脑皮质发育的许多重要方面。Wnts在皮质发育过程中如何与其调节因子相互作用仍不清楚。在此，我们表明Wnt7a和分泌型卷曲相关蛋白1（Sfrp1，Wnts的一种可溶性调节因子）在小鼠胚胎皮质神经祖细胞（NP）中共同表达。敲除小鼠体内的Wnt7a会因神经祖细胞数量减少和神经发生减少而导致小头畸形，并且Sfrp1与Wnt7a具有相反的作用。与Dickkopf-1（Dkk1）类似，Sfrp1会降低Wnt1和Wnt7a的活性。我们的结果表明，Wnt7a和Sfrp1发挥相反作用以确保发育中的皮质中神经祖细胞后代数量正常。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/f546f0e25c4a/fnmol-11-00247-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/7c9815218f04/fnmol-11-00247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/39448e6fca78/fnmol-11-00247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/2135ea698ae1/fnmol-11-00247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/069dc1ee2ddb/fnmol-11-00247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/54f5f1018d67/fnmol-11-00247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/f546f0e25c4a/fnmol-11-00247-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/7c9815218f04/fnmol-11-00247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/39448e6fca78/fnmol-11-00247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/2135ea698ae1/fnmol-11-00247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/069dc1ee2ddb/fnmol-11-00247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/54f5f1018d67/fnmol-11-00247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed7b/6056652/f546f0e25c4a/fnmol-11-00247-g006.jpg

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