scholarly journals Kv1.1 channels regulate early postnatal neurogenesis in mouse hippocampus via the TrkB signaling pathway

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Shu-Min Chou ◽  
Ke-Xin Li ◽  
Ming-Yueh Huang ◽  
Chao Chen ◽  
Yuan-Hung Lin King ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Multinomial Logistic Regression ◽  
Neural Progenitor ◽  
Cell Renewal ◽  
Postnatal Neurogenesis ◽  
Stem Cell Renewal ◽  
Mouse Hippocampus

In the postnatal brain, neurogenesis occurs only within a few regions, such as the hippocampal sub-granular zone (SGZ). Postnatal neurogenesis is tightly regulated by factors that balance stem cell renewal with differentiation, and it gives rise to neurons that participate in learning and memory formation (Anacker and Hen, 2017; Bond et al., 2015; Toda et al., 2019). The Kv1.1 channel, a voltage-gated potassium channel, was previously shown to suppress postnatal neurogenesis in the SGZ in a cell-autonomous manner. In this study, we clarified the physiological and molecular mechanisms underlying Kv1.1-dependent postnatal neurogenesis. First, we discovered that the membrane potential of neural progenitor cells is highly dynamic during development. We further established a multinomial logistic regression model for cell type classification based on the biophysical characteristics and corresponding cell markers. We found that loss of Kv1.1 channel activity causes significant depolarization of type 2b neural progenitor cells. This depolarization is associated with increased tropomyosin receptor kinase B (TrkB) signaling and proliferation of neural progenitor cells; suppressing TrkB signaling reduces the extent of postnatal neurogenesis. Thus, our study defines the role of the Kv1.1 potassium channel in regulating the proliferation of postnatal neural progenitor cells in the mouse hippocampus.

scholarly journals A protocol for isolation of fetal neural progenitor cells from mouse hippocampus

2014 ◽  
Vol 2 (2) ◽  
pp. 155-157
Author(s):  
O. Tsupykov
Keyword(s):  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Homogeneous Population ◽  
Mouse Hippocampus ◽  
Neural Stem Progenitor Cells ◽  
Percoll Density Gradient ◽  
Detailed Protocol

Culture of neural stem/progenitor cells are widely used to study the characteristics of these cells under controlled conditions in vitro as well as to study the cellular and molecular mechanisms of CNS diseases and develop strategies for their treatment.This paper provides a detailed protocol to isolate of fetal (E17-18) neural progenitor cells (NPCs) of mouse hippocampus. The technique is based on the use of centrifugation of hippocampal cells suspension in Percoll density gradient to obtain purified NPCs fractions. The cells are cultured in serum-free medium in a monolayer, which creates conditions for more equitable access of FGF-2 to the cells. This method provides a homogeneous population of undifferentiated progenitors from fetal mouse hippocampus.

scholarly journals NCAM regulates temporal specification of neural progenitor cells via profilin2 during corticogenesis

2019 ◽  
Vol 219 (1) ◽  
Author(s):  
Rui Huang ◽  
De-Juan Yuan ◽  
Shao Li ◽  
Xue-Song Liang ◽  
Yue Gao ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Cortical Neurons ◽  
Actin Polymerization ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Cortical Development ◽  
Neural Progenitor ◽  
Neural Cell Adhesion ◽  
Fate Decision ◽  
Temporal Specification

The development of cerebral cortex requires spatially and temporally orchestrated proliferation, migration, and differentiation of neural progenitor cells (NPCs). The molecular mechanisms underlying cortical development are, however, not fully understood. The neural cell adhesion molecule (NCAM) has been suggested to play a role in corticogenesis. Here we show that NCAM is dynamically expressed in the developing cortex. NCAM expression in NPCs is highest in the neurogenic period and declines during the gliogenic period. In mice bearing an NPC-specific NCAM deletion, proliferation of NPCs is reduced, and production of cortical neurons is delayed, while formation of cortical glia is advanced. Mechanistically, NCAM enhances actin polymerization in NPCs by interacting with actin-associated protein profilin2. NCAM-dependent regulation of NPCs is blocked by mutations in the profilin2 binding site. Thus, NCAM plays an essential role in NPC proliferation and fate decision during cortical development by regulating profilin2-dependent actin polymerization.

Dopamine D2 receptor stimulation promotes the proliferation of neural progenitor cells in adult mouse hippocampus

Neuroreport ◽  
2007 ◽  
Vol 18 (7) ◽  
pp. 659-664 ◽  
Author(s):  
Takeshi Hiramoto ◽  
Yasunari Kanda ◽  
Yasushi Satoh ◽  
Kunio Takishima ◽  
Yasuhiro Watanabe
Keyword(s):  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Adult Mouse ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Neural Progenitor ◽  
Receptor Stimulation ◽  
Dopamine D2 ◽  
Mouse Hippocampus

scholarly journals IGF-I instructs multipotent adult neural progenitor cells to become oligodendrocytes

2004 ◽  
Vol 164 (1) ◽  
pp. 111-122 ◽  
Author(s):  
Jenny Hsieh ◽  
James B. Aimone ◽  
Brian K. Kaspar ◽  
Tomoko Kuwabara ◽  
Kinichi Nakashima ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Single Molecule ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Protein Signaling ◽  
Adult Rat ◽  
Morphogenetic Protein ◽  
Modeling Analysis ◽  
Igf I

Adult multipotent neural progenitor cells can differentiate into neurons, astrocytes, and oligodendrocytes in the mammalian central nervous system, but the molecular mechanisms that control their differentiation are not yet well understood. Insulin-like growth factor I (IGF-I) can promote the differentiation of cells already committed to an oligodendroglial lineage during development. However, it is unclear whether IGF-I affects multipotent neural progenitor cells. Here, we show that IGF-I stimulates the differentiation of multipotent adult rat hippocampus-derived neural progenitor cells into oligodendrocytes. Modeling analysis indicates that the actions of IGF-I are instructive. Oligodendrocyte differentiation by IGF-I appears to be mediated through an inhibition of bone morphogenetic protein signaling. Furthermore, overexpression of IGF-I in the hippocampus leads to an increase in oligodendrocyte markers. These data demonstrate the existence of a single molecule, IGF-I, that can influence the fate choice of multipotent adult neural progenitor cells to an oligodendroglial lineage.

Trehalose as glucose surrogate in proliferation and cellular mobility of adult neural progenitor cells derived from mouse hippocampus

2019 ◽  
Vol 126 (11) ◽  
pp. 1485-1491
Author(s):  
Alexandra Bertl ◽  
Victor Brantl ◽  
Norbert Scherbaum ◽  
Dan Rujescu ◽  
Jens Benninghoff
Keyword(s):  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Mouse Hippocampus

scholarly journals Comparative Microarray Analysis of Proliferating and Differentiating Murine ENS Progenitor Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Peter Helmut Neckel ◽  
Roland Mohr ◽  
Ying Zhang ◽  
Bernhard Hirt ◽  
Lothar Just
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Developmental Dysplasia ◽  
Cellular Mechanisms ◽  
Differentiation Markers ◽  
Early Differentiation

Postnatal neural progenitor cells of the enteric nervous system are a potential source for future cell replacement therapies of developmental dysplasia like Hirschsprung’s disease. However, little is known about the molecular mechanisms driving the homeostasis and differentiation of this cell pool. In this work, we conducted Affymetrix GeneChip experiments to identify differences in gene regulation between proliferation and early differentiation of enteric neural progenitors from neonatal mice. We detected a total of 1333 regulated genes that were linked to different groups of cellular mechanisms involved in cell cycle, apoptosis, neural proliferation, and differentiation. As expected, we found an augmented inhibition in the gene expression of cell cycle progression as well as an enhanced mRNA expression of neuronal and glial differentiation markers. We further found a marked inactivation of the canonical Wnt pathway after the induction of cellular differentiation. Taken together, these data demonstrate the various molecular mechanisms taking place during the proliferation and early differentiation of enteric neural progenitor cells.

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.

Abstract 141: The Microrna 17-92 Cluster in Neural Progenitor Cells is Required for Stroke-induced Neurogenesis and Gliogenesis

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Wanlong Pan ◽  
Xianshuang Liu ◽  
Xiaoming Zhang ◽  
Xinli Wang ◽  
Jiani Hu ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Artery Occlusion ◽  
Tamoxifen Treatment ◽  
Oligodendrocyte Progenitor Cells ◽  
Factor Inhibitor

Background: Molecular mechanisms underlying stroke-induced neurogenesis have not been fully investigated. The microRNA 17-92 cluster (miR17-92) regulates proliferation and differentiation of adult neural progenitor cells (NPCs). The present study investigated whether the miR17-92 cluster in NPCs is required for stroke-induced neurogenesis. Methods and Results: Mice with inducible and conditional knockdown of the miR17-92 cluster in nestin lineage NPCs (nestin-CreER T2 /miR17-92 -/- , 17-92-cKO, n=9) and wild-type litters (WT, n=9) were treated by tamoxifen. Administration of tamoxifen resulted in more than 60% reduction of individual members of the miR-17-92 cluster (miR-17: 1.0 vs 0.4; miR-19a: 1.0 vs 0.3; miR-19b: 1.0 vs 0.2; miR-20a: 1.0 vs 0.4; miR-92a: 1.0 vs 0.4 fold in WT, p<0.05) in NPCs localized to the subventricular zone (SVZ). Two days after termination of tamoxifen treatment, these mice were subjected to permanent right middle cerebral artery occlusion (MCAO) and sacrificed 28 days post-MCAo. Compared to WT mice, 17-92-cKO mice exhibited significant (p<0.05) reduction of proliferation of NPCs measured by the number of Ki67 + cells (226±43 vs 471±100 cells/mm 2 ) and the number of DCX + neuroblasts (11±2% vs 24±4% ) in the ischemic SVZ. Cultured NPCs harvested from ischemic cKO mice showed significant (p<0.05) reduction of BrdU + cells (37±2% vs 61±4% WT , n=3/group), Tuj1 + neuroblasts (5±0.2% vs 9±0.4% ), GFAP + cells (33±3% vs 53±2% ), and NG2 + oligodendrocyte progenitor cells (OPCs, 3±0.1% vs 5±0.5%). These in vivo and in vitro data indicate that reduction of the miR17-92 cluster suppresses stroke-induced neurogenesis and gliogenesis. Western blot analysis showed that miR17-92 cKO significantly (p<0.05) increased and reduced a cytoskeleton-associated protein, Enigma homolog1 (ENH1, 1.6 vs 1.0 fold), and its down-stream transcription factor, inhibitor of differentiation1 (ID1, 1.0 vs 0.6 fold), respectively. ENH1 is a putative target of the miR17-92 cluster. Conclusion: Our data indicate that the miR17-92 cluster in adult nestin lineage NPCs is required for stroke-induced neurongenesis and gliogenesis, and that the miR17-92 cluster possibly targets ENH1/ID1 signaling.

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