Journal info
|
||||
Select Journal
Journals
Bratislava Medical Journal 2024 Ahead of print 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 Endocrine Regulations General Physiology and Biophysics Neoplasma Acta Virologica Studia Psychologica Cardiology Letters Psychológia a patopsych. dieťaťa Kovove Materialy-Metallic Materials Slovenská hudbaWebshop Cart
Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.
Bratislava Medical Journal Vol.115, No.4, p.203-208, 2014 |
||
Title: Phosphoinositid signal pathway mediate neurite outgrowth in PC12 cells by staurosporine | ||
Author: H. Zhaleh, M. Azadbakht, A. Bidmeshki Pour | ||
Abstract: Objectives: In previous studies, we showed that staurosporine uses intracellular calcium ions to affect cell death in PC12 cells. The bulk release of intracellular excessive Ca2+ from intracellular sources into cytosol contributes to neuronal apoptotic events, which in turn results in neuronal cell death. However, the mechanisms of Ca2+-induced neuronal cell death or neurite elongation is still unclear. Therefore, we investigated the relation between phosphoinositid signal pathway, intracellular calcium, and reactive oxygen species on one hand, with staurosporine-induced neurite outgrowth in PC12 cells on the other. Results: The inhibition of phospholipase C or IP3 receptor antagonist or phosphoinositid signal transduction antagonist produced cell death and suppressed neurite outgrowth by staurosporine in PC12 cells. The inhibition of these enzymes and pathway results in an increase in intracellular Ca2+ although subsequent hydroxyl radical (•OH) production began after inhibitors exposure. •OH production was significantly attenuated in inhibitor supplemented medium treatment, and it was dependent on the intracellular Ca2+ concentration. These data indicate that staurosporine activates phosphoinositid signal pathway while endoplasmic Ca2+, and subsequent •OH production are critical events in staurosporine-induced neurite outgrowth in PC12 cells. Conclusion: We conclude that the fact that staurosporine mobilizes Ca2+, probably via activating the subcellular compartment, is responsible for staurosporine-induced (Ca2+]i increase during neurite outgrowth in PC12 cells (Fig. 7, Ref. 30). T |
||
Keywords: endoplasmic reticulum, neurite outgrowth, staurosporine, PC12 cells. | ||
Year: 2014, Volume: 115, Issue: 4 | Page From: 203, Page To: 208 | |
doi:10.4149/BLL_2014_043 |
||
|
![]() |
|