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转化生长因子-β信号在出生后神经干细胞增殖和迁移中的细胞类型依赖性作用。

Cell type-dependent role of transforming growth factor-β signaling on postnatal neural stem cell proliferation and migration.

作者信息

Ware Kierra, Peter Joshua, McClain Lucas, Luo Yu

机构信息

Department of Molecular and Cellular Biosciences, University of Cincinnati, Cincinnati, OH, USA.

Neuroscience Graduate Program, University of Cincinnati, Cincinnati, OH, USA.

出版信息

Neural Regen Res. 2026 Mar 1;21(3):1151-1161. doi: 10.4103/NRR.NRR-D-24-00623. Epub 2025 Jan 29.

DOI:10.4103/NRR.NRR-D-24-00623
PMID:39885664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12296437/
Abstract

JOURNAL/nrgr/04.03/01300535-202603000-00039/figure1/v/2025-06-16T082406Z/r/image-tiff Adult neurogenesis continuously produces new neurons critical for cognitive plasticity in adult rodents. While it is known transforming growth factor-β signaling is important in embryonic neurogenesis, its role in postnatal neurogenesis remains unclear. In this study, to define the precise role of transforming growth factor-β signaling in postnatal neurogenesis at distinct stages of the neurogenic cascade both in vitro and in vivo , we developed two novel inducible and cell type-specific mouse models to specifically silence transforming growth factor-β signaling in neural stem cells in ( mGFAPcre - ALK5fl/fl - Ai9 ) or immature neuroblasts in ( DCXcreERT2 - ALK5fl/fl - Ai9 ). Our data showed that exogenous transforming growth factor-β treatment led to inhibition of the proliferation of primary neural stem cells while stimulating their migration. These effects were abolished in activin-like kinase 5 (ALK5) knockout primary neural stem cells. Consistent with this, inhibition of transforming growth factor-β signaling with SB-431542 in wild-type neural stem cells stimulated proliferation while inhibited the migration of neural stem cells. Interestingly, deletion of transforming growth factor-β receptor in neural stem cells in vivo inhibited the migration of postnatal born neurons in mGFAPcre - ALK5fl/fl - Ai9 mice, while abolishment of transforming growth factor-β signaling in immature neuroblasts in DCXcreERT2 - ALK5fl/fl - Ai9 mice did not affect the migration of these cells in the hippocampus. In summary, our data supports a dual role of transforming growth factor-β signaling in the proliferation and migration of neural stem cells in vitro . Moreover, our data provides novel insights on cell type-specific-dependent requirements of transforming growth factor-β signaling on neural stem cell proliferation and migration in vivo .

摘要

《期刊》/nrgr/04.03/01300535 - 202603000 - 00039/图1/v/2025 - 06 - 16T082406Z/图像 - tiff 成年神经发生持续产生对成年啮齿动物认知可塑性至关重要的新神经元。虽然已知转化生长因子 - β信号在胚胎神经发生中很重要，但其在出生后神经发生中的作用仍不清楚。在本研究中，为了在体外和体内明确转化生长因子 - β信号在神经发生级联不同阶段的出生后神经发生中的精确作用，我们开发了两种新型的可诱导且细胞类型特异性的小鼠模型，以特异性沉默神经干细胞（mGFAPcre - ALK5fl/fl - Ai9）或未成熟神经母细胞（DCXcreERT2 - ALK5fl/fl - Ai9）中的转化生长因子 - β信号。我们的数据表明，外源性转化生长因子 - β处理导致原代神经干细胞增殖受到抑制，同时刺激其迁移。这些效应在激活素样激酶5（ALK5）敲除的原代神经干细胞中被消除。与此一致，在野生型神经干细胞中用SB - 43,154抑制转化生长因子 - β信号刺激了增殖，同时抑制了神经干细胞的迁移。有趣的是，在体内神经干细胞中缺失转化生长因子 - β受体会抑制mGFAPcre - ALK5fl/fl - Ai9小鼠中出生后神经元的迁移，而在DCXcreERT,2 - ALK5fl/fl - Ai9小鼠的未成熟神经母细胞中消除转化生长因子 - β信号并不影响这些细胞在海马体中的迁移。总之，我们的数据支持转化生长因子 - β信号在体外神经干细胞增殖和迁移中的双重作用。此外，我们的数据为转化生长因子 - β信号在体内神经干细胞增殖和迁移中对细胞类型特异性依赖的需求提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/0c612667678b/NRR-21-1151-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/7726ad269a1a/NRR-21-1151-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/3a9a405e4f99/NRR-21-1151-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/33f1fde96e81/NRR-21-1151-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/658ee0a69ef8/NRR-21-1151-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/924a866e7e8c/NRR-21-1151-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/f351f289d82f/NRR-21-1151-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/0c612667678b/NRR-21-1151-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/7726ad269a1a/NRR-21-1151-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/3a9a405e4f99/NRR-21-1151-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/33f1fde96e81/NRR-21-1151-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/658ee0a69ef8/NRR-21-1151-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/924a866e7e8c/NRR-21-1151-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/f351f289d82f/NRR-21-1151-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de08/12296437/0c612667678b/NRR-21-1151-g008.jpg

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