P48. Formation of blood vessels is controlled by neural progenitor cells in the central nervous system

2010 ◽  
Vol 80 ◽  
pp. S33
Author(s):  
Teruaki Takahashi ◽  
Yuta Takase ◽  
Ryosuke Tadokoro ◽  
Yoshiko Takahashi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Vessels ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
The Central Nervous System

scholarly journals Patterning of blood vessels is controlled by neural progenitor cells in the central nervous system

2010 ◽  
Vol 344 (1) ◽  
pp. 523-524
Author(s):  
Teruaki Takahashi ◽  
Ryosuke Tadokoro ◽  
Yuta Takase ◽  
Yoshiko Takahashi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Vessels ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
The Central Nervous System

scholarly journals Neural progenitor cells mediated by H2A.Z.2 regulate microglial development via Cxcl14 in the embryonic brain

2019 ◽  
Vol 116 (48) ◽  
pp. 24122-24132 ◽  
Author(s):  
Zhongqiu Li ◽  
Yanxin Li ◽  
Jianwei Jiao
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Ventricular Zone ◽  
Neural Progenitor ◽  
The Central Nervous System ◽  
Microglial Development

Microglia, the resident immune cells of the central nervous system, play an important role in the brain. Microglia have a special spatiotemporal distribution during the development of the cerebral cortex. Neural progenitor cells (NPCs) are the main source of neural-specific cells in the early brain. It is unclear whether NPCs affect microglial development and what molecular mechanisms control early microglial localization. H2A.Z.2, a histone variant of H2A, has a key role in gene expression regulation, genomic stability, and chromatin remodeling, but its function in brain development is not fully understood. Here, we found that the specific deletion of H2A.Z.2 in neural progenitor cells led to an abnormal increase in microglia in the ventricular zone/subventricular zone (VZ/SVZ) of the embryonic cortex. Mechanistically, H2A.Z.2 regulated microglial development by incorporating G9a into the promoter region of Cxcl14 and promoted H3k9me2 modification to inhibit the transcription of Cxcl14 in neural progenitor cells. Meanwhile, we found that the deletion of H2A.Z.2 in microglia itself had no significant effect on microglial development in the early cerebral cortex. Our findings demonstrate a key role of H2A.Z.2 in neural progenitor cells in controlling microglial development and broaden our knowledge of 2 different types of cells that may affect each other through crosstalk in the central nervous system.

scholarly journals RalGAPα1is dispensable for embryonic cortical morphogenesisin mice

2021 ◽  
Author(s):  
Yingqian Xia ◽  
Chaoli Huang ◽  
Sangsang Zhu ◽  
Qiaoli Chen ◽  
Guiquan Chen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Development ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Cortical Development ◽  
Neural Progenitor ◽  
Conditional Knockout ◽  
Deletion Syndrome ◽  
The Central Nervous System

Abstract Background: Cortical morphogenesis is a complex process and involves a large number of genes. RalGAPα1 gene (also called Tulip1 ), mapped to chromosome 14q13.2, is a candidate gene for the 14q13 deletion syndrome associated with delayed brain development. However, it remains unknown whether RalGAPα1 directly regulates cortical development. Methods: To address the above question, we generated neural progenitor cells (NPCs) specific RalGAPα1 conditional knockout (cKO) mice through crossing RalGAPα1 f/f to Nestin-Cre transgenic (Tg) mice in which the Cre recombinase is expressed in neural progenitor cells and derived neurons in the central nervous system (CNS) since very early stage of development. Morphological, biochemistry and immunohistochemistry (IHC) methods were used to evaluate brain development. Results: We found that the brain size, shape and cortical laminations were comparable between control and RalGAPα1 cKO mice. Moreover, the populations and proliferations of NPCs in the ventricular and subventricular zones were not different between control and RalGAPα1 cKO cortices. Conclusions: Inactivation of RalGAPα1 in the central nervous system in murine model does not significantly affect the embryonic cortical development. Keywords: RalGAPα1 ; cortical development; neural progenitor cells; neurodevelopmental disease

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