Implication of cyclooxygenase-2 on enhanced proliferation of neural progenitor cells in the adult mouse hippocampus after ischemia

2003 ◽  
Vol 72 (4) ◽  
pp. 461-471 ◽  
Author(s):  
Tsutomu Sasaki ◽  
Kazuo Kitagawa ◽  
Shiro Sugiura ◽  
Emi Omura-Matsuoka ◽  
Shigeru Tanaka ◽  
...  
Neuroreport ◽  
2007 ◽  
Vol 18 (7) ◽  
pp. 659-664 ◽  
Author(s):  
Takeshi Hiramoto ◽  
Yasunari Kanda ◽  
Yasushi Satoh ◽  
Kunio Takishima ◽  
Yasuhiro Watanabe

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

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Shu-Min Chou ◽  
Ke-Xin Li ◽  
Ming-Yueh Huang ◽  
Chao Chen ◽  
Yuan-Hung Lin King ◽  
...  

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.


Author(s):  
Miguel V. Guerra ◽  
Matías I. Cáceres ◽  
Andrea Herrera-Soto ◽  
Sebastián B. Arredondo ◽  
Manuel Varas-Godoy ◽  
...  

In the dentate gyrus of the adult hippocampus new neurons are generated from neural precursor cells through different stages including proliferation and differentiation of neural progenitor cells and maturation of newborn neurons. These stages are controlled by the expression of specific transcription factors and epigenetic mechanisms, which together orchestrate the progression of the neurogenic process. However, little is known about the involvement of histone posttranslational modifications, a crucial epigenetic mechanism in embryonic neurogenesis that regulates fate commitment and neuronal differentiation. During embryonic development, the repressive modification trimethylation of histone H3 on lysine 9 (H3K9me3) contributes to the cellular identity of different cell-types. However, the role of this modification and its H3K9 methyltransferases has not been elucidated in adult hippocampal neurogenesis. We determined that during the stages of neurogenesis in the adult mouse dentate gyrus and in cultured adult hippocampal progenitors (AHPs), there was a dynamic change in the expression and distribution of H3K9me3, being enriched at early stages of the neurogenic process. A similar pattern was observed in the hippocampus for the dimethylation of histone H3 on lysine 9 (H3K9me2), another repressive modification. Among H3K9 methyltransferases, the enzymes Suv39h1 and Suv39h2 exhibited high levels of expression at early stages of neurogenesis and their expression decreased upon differentiation. Pharmacological inhibition of these enzymes by chaetocin in AHPs reduced H3K9me3 and concomitantly decreased neuronal differentiation while increasing proliferation. Moreover, Suv39h1 and Suv39h2 knockdown in newborn cells of the adult mouse dentate gyrus by retrovirus-mediated RNA interference impaired neuronal differentiation of progenitor cells. Our results indicate that H3K9me3 and H3K9 methyltransferases Suv39h1 and Suv39h2 are critically involved in the regulation of adult hippocampal neurogenesis by controlling the differentiation of neural progenitor cells.


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