Calcium overload is essential for the acceleration of staurosporine-induced cell death following neuronal differentiation in PC12 cells

Seo, Su Ryeon; Seo, Jeong Taeg

doi:10.3858/emm.2009.41.4.030

Cited by 28 publications

(23 citation statements)

References 33 publications

(39 reference statements)

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“…It was demonstrated that neurite outgrowth in PC12 by staurosporine is induced via the Ca 2+ -signal transduction pathway by the Ca 2+ infl uxes through endoplasmic reticulum channels. On the other hand, recent study showed that staurosporine leads to intracellular calcium overload, which induces apoptosis in PC12 cells (6). In the percent study, we showed that inhibition of IP3R and PLCγ caused a large increase in (Ca We reported previously that staurosporine can induce neurite outgrowth in PC12 cells and that this apoptosis can be blocked by reducing extracellular calcium stores (12).…”

Section: Discussionmentioning

confidence: 72%

Phosphoinositid signal pathway mediate neurite outgrowth in PC12 cells by staurosporine

Zhaleh¹,

Azadbakht²,

Pour³

2014

BLL

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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 Ca 2+ from intracellular sources into cytosol contributes to neuronal apoptotic events, which in turn results in neuronal cell death. However, the mechanisms of Ca 2+ -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 Ca 2+ although subsequent hydroxyl radical (•OH) production began after inhibitors exposure.•OH production was signifi cantly attenuated in inhibitor supplemented medium treatment, and it was dependent on the intracellular Ca 2+ concentration. These data indicate that staurosporine activates phosphoinositid signal pathway while endoplasmic Ca 2+, 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). Text in PDF www.elis.sk.

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Section: Discussionmentioning

confidence: 72%

Phosphoinositid signal pathway mediate neurite outgrowth in PC12 cells by staurosporine

Zhaleh¹,

Azadbakht²,

Pour³

2014

BLL

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“…homeostasis of differentiated PC12 cells. Seo and Seo [59] found that the anti-apoptotic Bcl-2 family member Bcl-X L prevented STS-induced neuronal cell death by interfering with Ca 2? -mediated apoptotic signals by inhibiting Ca 2?…”

Section: Discussionmentioning

confidence: 99%

Multiple alphaII-spectrin breakdown products distinguish calpain and caspase dominated necrotic and apoptotic cell death pathways

et al. 2009

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Apoptosis and oncotic necrosis in neuronal and glial cells have been documented in many neurological diseases. Distinguishing between these two major types of cell death in different neurological diseases is needed in order to better reveal the injury mechanisms so as to open up opportunities for therapy development. Accumulating evidence suggests apoptosis and oncosis epitomize the extreme ends of a broad spectrum of morphological and biochemical events. Biochemical markers that can distinguish between the calpain and caspase dominated types of cell death would help in this process. In this study, three chemical agents, maitotoxin (MTX), staurosporine (STS) and thylenediaminetetraacetic acid (EDTA), were used to induce different types of cell death in PC12 neuronal-like cells. MTX-induced necrosis, as determined by the increased levels of calpain-specific cleaved fragments of spectrin by antibodies specific to the calpain-cleaved 150 kDa alphaII-spectrin breakdown product (SBDP150) and 145 kDa alphaII-spectrin breakdown product (SBDP145). In this paradigm, there were no detectable SBDP150i and SBDP120 fragments as determined by antibodies specific to the caspase-cleaved specific fragments similar to those seen in the EDTA-mediated apoptotic PC-12 cells. In contrast to the calpain specific MTX necrosis treatment and the caspase EDTA apoptotic treatment is the STS treatment which induced both proteases as shown by the increase in all the SBDP fragments. Furthermore, compared to SBDP150, SBDP145 appears to be a more specific and sensitive biomarker for calpain activation. Taken together, our results suggested calpains and caspases which dominate the two major types of cell death could be independently discriminated by specifically examining the multiple alphaII-spectrin cleavage breakdown products.

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“…Many important mechanisms involved in apoptosis have been determined using STS or mycotoxin, a general protein kinase inhibitor that triggers apoptosis in model cell lines (Xia et al, 1995;Jacobsen et al, 1996;Seo and Seo, 2009). The intracellular signaling of STS induced apoptosis is dependent on cell type.…”

Section: Staurosporine (Sts) Induces Neuronal Apoptosis In H19-7 Cellmentioning

confidence: 99%

Neuroprotection signaling pathway of nerve growth factor and brain-derived neurotrophic factor against staurosporine induced apoptosis in hippocampal H19-7 cells

et al. 2010

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Neurotrophins protect neurons against excitotoxicity; however the signaling mechanisms for this protection remain to be fully elucidated. Here we report that activation of the phosphatidyl inositol 3 kinase (PI3K)/Akt pathway is critical for protection of hippocampal cells from staurosporine (STS) induced apoptosis, characterized by nuclear condensation and activation of the caspase cascade. Both nerve growth factor (NGF) and brain-derived growth factor (BDNF) prevent STS-induced apoptotic morphology and caspase-3 activity by upregulating phosphorylation of the tropomyosin receptor kinase (Trk) receptor. Inhibition of Trk receptor by K252a altered the neuroprotective effect of both NGF and BDNF whereas inhibition of the p75 neurotrophin receptor (p75NTR) had no effect. Impairment of the PI3K/Akt pathway or overexpression of dominant negative (DN)-Akt abolished the protective effect of both neurotrophins, while active Akt prevented cell death. Moreover, knockdown of Akt by si-RNA was able to block the survival effect of both NGF and BDNF. Thus, the survival action of NGF and BDNF against STS-induced neurotoxicity was mediated by the activation of PI3K/Akt signaling through the Trk receptor.

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Calcium overload is essential for the acceleration of staurosporine-induced cell death following neuronal differentiation in PC12 cells

Abstract: Abstract

Cited by 28 publications

References 33 publications

Phosphoinositid signal pathway mediate neurite outgrowth in PC12 cells by staurosporine

Phosphoinositid signal pathway mediate neurite outgrowth in PC12 cells by staurosporine

Multiple alphaII-spectrin breakdown products distinguish calpain and caspase dominated necrotic and apoptotic cell death pathways

Neuroprotection signaling pathway of nerve growth factor and brain-derived neurotrophic factor against staurosporine induced apoptosis in hippocampal H19-7 cells

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