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Author Salozhin, S. V. ♦ Borodiva, A. A. ♦ Kvichanskii, A. A. ♦ Mikhailova, T. V. ♦ Spivak, Yu. S. ♦ Bolshakov, A. P.
Source SpringerLink
Content type Text
Publisher Pleiades Publishing
File Format PDF
Copyright Year ©2017
Language English
Subject Domain (in DDC) Technology ♦ Medicine & health
Subject Keyword pheochromocytoma PC12 ♦ neuronal culture ♦ caspase-3 ♦ serpinb1a ♦ nerve growth factor ♦ Neurosciences
Abstract It was shown that serpinb1a is expressed during differentiation of PC12 cells induced by nerve growth factor (NGF). Here, we found that overexpression of serpinb1a in PC12 cells weakly but significantly increases PC12 survival during staurosporine-induced apoptosis. Immunoprecipitation of serpinb1a after its overexpression in PC12 showed that this protein interacts with active caspase-3 in both resting cells and cells that were stimulated by staurosporine. NGF-induced PC12 differentiation resulted in the formation of outgrowths and a considerable increase in caspase-3 activity in 24 h after the beginning of NGF treatment. This increase in the activity of caspase-3 lasted for at least 48 h. Overexpression of serpinb1a in PC12 cells suppressed the growth of neurites during NGF-induced differentiation; this effect was observed only at 48 h. Experiments performed with primary cultures of neocortical and hippocampal neurons showed that serpinb1a overexpression results in relatively weak changes in morphology: serpinb1a decreased the number of secondary dendrites in the cortical and average length of secondary dendrites in hippocampal neurons. The results of the experiments suggests that serpinb1a may interact with caspase-3 and influence the differentiation of PC12 cells but not neuronal cells.
ISSN 18197124
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG
Learning Resource Type Article
Publisher Date 2017-03-25
Publisher Place Moscow
e-ISSN 18197132
Journal Neurochemical Journal
Volume Number 11
Issue Number 1
Page Count 8
Starting Page 23
Ending Page 30


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Source: SpringerLink