Effect of dibutyryl cAMP and several reagents on apoptosis in PC12 cells induced by a sialoglycopeptide from bovine brain

Kobayashi, Yôko; Shinozawa, Takao

doi:10.1016/s0006-8993(97)01072-x

Cited by 12 publications

(7 citation statements)

References 39 publications

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“…This effect is probably not due to an action of AZA-1 on the cAMP pathway since several studies have demonstrated that elevating the cAMP level attenuated cell death induced by neurotoxicity, [30]. Furthermore, the increase of intracellular levels of cAMP promotes cell survival or delays cell death induced by various conditions [31][32][33].…”

Section: Discussionmentioning

confidence: 97%

The c-Jun-N-Terminal Kinase is Involved in the Neurotoxic Effect of Azaspiracid-1

Vale¹,

Gómez-Limia²,

Nicolaou

et al. 2007

Cell Physiol Biochem

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Aims: Azaspiracids (AZAs) are marine phycotoxins with an unknown mechanism of action, recently implicated in human intoxications. The predominant analog in nature, AZA-1 targets several organs in vivo, including the central nervous system and exhibits high neurotoxicity in vitro. Methods: We used pharmacological tools to inhibit the cytotoxic effect of the toxin in primary cultured neurons. Immunocytochemical techniques in combination with confocal microscopy were employed to examine the cellular mechanisms involved in the neurotoxic effect of AZA-1. Results: Several targets for azaspiracid-induced neurotoxicity, specifically the cAMP pathway, or protein kinase C and phosphatidylinositol 3-kinase activation were excluded. Interestingly, the specific c-Jun-N-terminal protein kinase (JNK) inhibitor SP 600125 protected cultured neurons against AZA-induced cytotoxicity. Immunocytochemistry experiments showed that AZA-1 increased the amount of phosphorylated JNK and caused nuclear translocation of the active protein that was prevented by SP 600125. Conclusion: Our data constitute the relationship between azaspiracid-induced cytotoxicity and specific modifications in cellular transduction signals, specifically we found that JNK activation is associated with the cytotoxic effect of the toxin. These results should provide the basis to identify the mechanism of action of this group of toxins.

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Section: Discussionmentioning

confidence: 97%

The c-Jun-N-Terminal Kinase is Involved in the Neurotoxic Effect of Azaspiracid-1

Vale¹,

Gómez-Limia²,

Nicolaou

et al. 2007

Cell Physiol Biochem

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“…The viability of the PC12 cells was determined using the MTT reagent (Kobayashi and Shinozawa 1997). The cells were seeded at a density of 1 9 10 4 cells/well in 96-well polyethyleneimine-coated plates at 1 or 2 days before the experiment.…”

Section: Pc12 Cell Viability Assaymentioning

confidence: 99%

Contribution of Intracellular Ca2+ Concentration and Protein Dephosphorylation to the Induction of Dopamine Release from PC12 cells by the Green Odor Compound Hexanal

2009

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n-Hexanal (hexanal), a straight-chain six-carbon aldehyde, is mainly present in plants. Hexanal strongly affects the release of dopamine from rat striatal slices and rat pheochromocytoma (PC12) cells. In this study, we attempted to clarify the mechanism underlying the regulation of dopamine release by hexanal by using PC12 cells, which have the ability to synthesize, store, and release dopamine. The stimulation of PC12 cells with hexanal enhanced dopamine release in a time- and dose-dependent manner. Dopamine release was partially inhibited by pretreatment of the cells with BAPTA-AM, a cell-permeable Ca2+ chelator. In addition, the intracellular Ca2+ concentration was found to slowly increase after hexanal stimulation. Furthermore, the Src tyrosine kinase inhibitor PP2 partially inhibited hexanal-induced dopamine release. However, the levels of phosphorylated proteins decreased after hexanal stimulation. Hexanal stimulated the release of only a small amount of dopamine from reserpine-treated PC12 cells, in which the vesicular dopamine was depleted. These findings suggest that both an increase in the intracellular Ca2+ concentration and the dephosphorylation of phosphorylated proteins might be required for hexanal-stimulated release of dopamine, and that the dopamine released because of hexanal stimulation mainly comes from the dopamine vesicles. This study showed the cellular events that occurred in PC12 cells after stimulation of hexanal. Furthermore, it is important to examine the relationship between the cellular functions and the physiological effects of hexanal on dopamine release.

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“…Activation of the cAMP signalling and/or increased CREB phosphorylation could contribute to the neuroprotective eects of estradiol, as activation of the cAMP pathway is associated with decreased susceptibility of neuronal cell to apoptotic signals [14,23,63,64,97]. Further, Hanson et al [52] have demonstrated that elevation of cAMP is sucient to enhance the survival of spinal motor neurons in culture.…”

Section: Activation Of Camp±pka±creb Pathwaymentioning

confidence: 99%

Neuroprotective effects of estrogens: potential mechanisms of action

Green

Simpkins

2000

Intl J of Devlp Neuroscience

477

286

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Epidemiological studies associate post-menopausal estrogen use with a reduction in risk of Alzheimer's disease, a reduction in risk of Parkinson's disease, and death from stroke. The neuroprotective efficacy of estrogens have been well described and may contribute to these clinical effects. Estrogen-mediated neuroprotection has been described in several neuronal culture model systems with toxicities including serum-deprivation, beta-amyloid-induced toxicity, excitotoxicity, and oxidative stress. In animal models, estrogens have been shown to attenuate neuronal death in rodent models of cerebral ischemia, traumatic injury, and Parkinson's disease. Although estrogens are known to exert several direct effects on neurons, the cellular mechanisms behind the neuroprotective efficacy of the steroid are only beginning to be elucidated. In this review, we summarize the data supporting a neuroprotective role for estrogens in both culture and animal models and discuss neuronal effects of estrogens that may contribute to the neuroprotective effects. These effects include activation of the nuclear estrogen receptor, altered expression of bcl-2 and related proteins, activation of the mitogen activated kinase pathway, activation of cAMP signal transduction pathways, modulation of intracellular calcium homeostasis, and direct antioxidant activity.

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Effect of dibutyryl cAMP and several reagents on apoptosis in PC12 cells induced by a sialoglycopeptide from bovine brain

Cited by 12 publications

References 39 publications

The c-Jun-N-Terminal Kinase is Involved in the Neurotoxic Effect of Azaspiracid-1

The c-Jun-N-Terminal Kinase is Involved in the Neurotoxic Effect of Azaspiracid-1

Contribution of Intracellular Ca2+ Concentration and Protein Dephosphorylation to the Induction of Dopamine Release from PC12 cells by the Green Odor Compound Hexanal

Neuroprotective effects of estrogens: potential mechanisms of action

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