scholarly journals Protease Omi facilitates neurite outgrowth in mouse neuroblastoma N2a cells by cleaving transcription factor E2F1

2015 ◽  
Vol 36 (8) ◽  
pp. 966-975 ◽  
Author(s):  
Qi Ma ◽  
Qing-song Hu ◽  
Ran-jie Xu ◽  
Xue-chu Zhen ◽  
Guang-hui Wang
Keyword(s):  
Transcription Factor ◽  
Neurite Outgrowth ◽  
Mouse Neuroblastoma ◽  
N2a Cells ◽  
Transcription Factor E2f1

Effects of avermectins on neurite outgrowth in differentiating mouse neuroblastoma N2a cells

2010 ◽  
Vol 192 (2) ◽  
pp. 206-211 ◽  
Author(s):  
Ying-Jian Sun ◽  
Ding-Xin Long ◽  
Wei Li ◽  
Wei-Yuan Hou ◽  
Yi-Jun Wu ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Mouse Neuroblastoma ◽  
N2a Cells

Propofol Pretreatment Prevents Oxygen-Glucose Deprivation/Reoxygenation (OGD/R)-induced Inflammation Through Nuclear Transcription Factor κB (NF-κB) Pathway in Neuroblastoma Cells

2020 ◽  
Vol 17 (1) ◽  
pp. 27-34
Author(s):  
Fang Hu ◽  
Jianhua Jiang ◽  
Guocan Yu ◽  
Hongcheng Zang ◽  
Haoliang Sun
Keyword(s):  
Transcription Factor ◽  
Protein Expression ◽  
Western Blot ◽  
Neuroblastoma Cells ◽  
Glucose Deprivation ◽  
Inflammatory Factors ◽  
Oxygen Glucose Deprivation ◽  
Nuclear Transcription Factor ◽  
Mouse Neuroblastoma ◽  
N2a Cells

Background: Inflammation is one of the causes of neuroblastoma progression. Propofol attenuates inflammation by repressing nuclear transcription factor κB (NF-κB) in different diseases. But its effect on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced inflammation is not known. Objective: This study investigated the role and mechanism of action of propofol on OGD/Rinduced inflammation in mouse N2A neuroblastoma cells. Methods: MTT was performed on mouse neuroblastoma cells N2A to assess and select the maximum safe dose of propofol. Next, N2A cells were pretreated with propofol and then, exposed to the OGD condition for 3 h and reoxygenated for 6 h. The content of the inflammatory factors, interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), in the medium was measured by ELISA, while their protein expression was detected by western blot and immunofluorescence. The protein expression of P65, p-P65, IKBα and p-IKBα belonging to the NF-κB pathway was also determined by western blot in N2A cells. To further confirm the mechanism of propofol on OGD/R-induced inflammation in mouse N2A cells, P65 was over-expressed and the above experiments were repeated. Results: Propofol did not affect cell viability of N2A cells even at the maximum concentration used (30 µM), thus, 30 µM of propofol was selected to perform our experiments. Besides, OGD/R induced inflammation and activation of NF-κB pathway with increased p-P65 and p-IKBα expression, and propofol pretreatment inhibited OGD/R induced inflammation and activation of NF-κB pathway in N2A cells. Over-expression of P56 abolished the effects of propofol on OGD/Rinduced inflammation and activation of NF-κB pathway in N2A cells. Conclusion: Our work demonstrated for the first time that propofol pretreatment ameliorated OGD/R induced inflammation via NF-κB pathway modulation in mouse neuroblastoma N2A cells, indicating that propofol might be considered as a potential therapeutic approach to reduce inflammation in neuroblastoma.

scholarly journals Expression of MicroRNA-29a Regulated by Yes-Associated Protein Modulates the Neurite Outgrowth in N2a Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Chunye Tan ◽  
Changlin Yu ◽  
Zhiwen Song ◽  
Hongjun Zou ◽  
Xu Xu ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Strong Association ◽  
In Silico Analysis ◽  
Luciferase Reporter ◽  
N2a Cells ◽  
Chip Experiment ◽  
High Level ◽  
Phosphatase And Tensin Homologue ◽  
Opposite Tendency ◽  
Silico Analysis

Yes-associated protein (YAP) is proved to increase miR-29a in the present study, but the relevant molecular mechanism is not clear. Also, growing evidence indicates that the high-level miR-29a promotes the neurite outgrowth by decreasing PTEN (phosphatase and tensin homologue deleted on chromosome 10). Results show that the expression of miR-29a increases but the PTEN decreases during transfecting the N2a cells with the YAP plasmid. Meanwhile, the advancement of neurite outgrowth is presented via using multiple methods to detect the expression of GAP-43 and NF-200, which have a strong association with neurite outgrowth. The expression of miR-29a, GAP-43, and NF-200 shows an opposite tendency compared to the PTEN when YAP is downregulated. By treating N2a cells with miR-29a mimic and inhibitor, we also find the same conclusion. For in silico analysis of miR-29a, its promoter may have a binding site for YAP. Based on a luciferase reporter assay and a chromatin immunoprecipitation (ChIP) experiment, we demonstrate that YAP could increase the expression of miR-29a by targeting the promoter of miR-29a. In conclusion, the results identify that YAP promotes the neurite outgrowth via targeting the promoter of miR-29a, and it may be an effective therapeutic medicine for the neural disease.

Goosecoid suppresses cell growth and enhances neuronal differentiation of PC12 cells

2000 ◽  
Vol 113 (15) ◽  
pp. 2705-2713
Author(s):  
K. Sawada ◽  
Y. Konishi ◽  
M. Tominaga ◽  
Y. Watanabe ◽  
J. Hirano ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Neurite Outgrowth ◽  
Neuronal Differentiation ◽  
Pc12 Cells ◽  
Mammalian Cells ◽  
Homeobox Gene ◽  
S Phase ◽  
Bhlh Transcription Factor ◽  
Spemann Organizer

In all vertebrate species, the homeobox gene goosecoid serves as a marker of the Spemann organizer tissue. One function of the organizer is the induction of neural tissue. To investigate the role of goosecoid in neuronal differentiation of mammalian cells, we have introduced goosecoid into PC12 cells. Expression of goosecoid resulted in reduced cell proliferation and enhanced neurite outgrowth in response to NGF. Expression of goosecoid led to a decrease in the percentage of S-phase cells and to upregulation of the expression of the neuron-specific markers MAP-1b and neurofilament-L. Analysis of goosecoid mutants revealed that these effects were independent of either DNA binding or homodimerization of Goosecoid. Coexpression of the N-terminal portion of the ets transcription factor PU.1, a protein that can bind to Goosecoid, repressed neurite outgrowth and rescued the proliferation of PC12 cultures. In contrast, expression of the bHLH transcription factor HES-1 repressed goosecoid-mediated neurite outgrowth without changing the proportion of S-phase cells. These results suggest that goosecoid is involved in neuronal differentiation in two ways, by slowing the cell cycle and stimulating neurite outgrowth, and that these two events are separately regulated.

GSK-3β activation mediates Nogo-66-induced inhibition of neurite outgrowth in N2a cells

2011 ◽  
Vol 505 (2) ◽  
pp. 165-170 ◽  
Author(s):  
Jian-ying Shen ◽  
Xu-xia Yi ◽  
Nan-xiang Xiong ◽  
Hai-jun Wang ◽  
Xiao-wei Duan ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
N2a Cells ◽  
Gsk 3Β

scholarly journals The Transcription Factor E2F1 Modulates Apoptosis of Neurons

2001 ◽  
Vol 75 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Sheng T. Hou ◽  
Debbie Callaghan ◽  
Marie-Christine Fournier ◽  
Irene Hill ◽  
Liping Kang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factor E2f1
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