NMDA-sensitive neurons profoundly influence delayed staurosporine-induced apoptosis in rat mixed cortical neuronal cultures

Thomas, Craig E.; Mayle, Douglas A.

doi:10.1016/s0006-8993(00)02834-1

Cited by 15 publications

(7 citation statements)

References 28 publications

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“…Caspase-3 activity has been consistently observed after exposure to staurosporine in cortical neurons (Moore et al, 2002;Thomas and Mayle, 2000). In the present study, we found activation of caspase-3 after staurosporine exposure.…”

Section: Discussionsupporting

confidence: 74%

In vitro and in vivo neuroprotective effect and mechanisms of glabridin, a major active isoflavan from Glycyrrhiza glabra (licorice)

et al. 2008

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Section: Discussionsupporting

confidence: 74%

In vitro and in vivo neuroprotective effect and mechanisms of glabridin, a major active isoflavan from Glycyrrhiza glabra (licorice)

et al. 2008

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“…Cytotoxicity assay It has been reported that lactose dehydrogenase (LDH) leakage not only occurs during necrosis, but also during the process of apoptosis [24,25] . Since 3-MA interferes with the MTT assay, LDH leakage was assessed as an index of cell death after the cotreatment of As 2 O 3 and 3-MA or NH 4 Cl.…”

Section: Methodsmentioning

confidence: 99%

Dynamic effects of autophagy on arsenic trioxide-induced death of human leukemia cell line HL60 cells

et al. 2008

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Aim: To evaluate the contribution of an autophagic mechanism to the As 2 O 3 -induced death of human acute myeloid leukaemia cell line HL60 cells. Methods: The growth inhibition of HL60 cells induced by As 2 O 3 was assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide colorimetric assay. The activation of autophagy was determined with monodansylcadaverine labeling and transmission electron microscope. The role of autophagy in the As 2 O 3 -induced death of HL60 cells was assessed using autophagic and lysosomal inhibitors. Immunofluorescence, flow cytometry, and Western blot analysis were used to study the apoptotic and autophagic mechanisms. Results: After treatment with As 2 O 3 , the proliferation of HL60 cells was significantly inhibited and the formation of autophagosomes increased. The blockade of autophagy maturation with the autophagy-specific inhibitor 3-methyladenine (3-MA) or the lysosome-neutralizing agent NH 4 Cl 1 h before As 2 O 3 potentiated the As 2 O 3 -induced death of HL60 cells. In contrast, 3-MA attenuated As 2 O 3 -induced death when administered 30 min after As 2 O 3 . 3-MA and NH 4 Cl also inhibited As 2 O 3 -induced upregulation of microtubule-associated protein 1 light chain 3, the protein required for autophagy in mammalian cells. Following As 2 O 3 , lysosomes were activated as indicated by increased levels of cathepsins B and L. The apoptotic response of HL60 cells to As 2 O 3 was suggested by the collapse of mitochondrial membrane potential, release of cytochrome c from mitochondria, and the activation of caspase-3. Pretreatment with 3-MA prior to As 2 O 3 amplified these apoptotic signals, while posttreatment with 3-MA 30 min after As 2 O 3 attenuated the apoptotic pathways. Conclusion: Autophagy plays complex roles in the As 2 O 3 -induced death of HL60 cells; it inhibits As 2 O 3 -induced apoptosis in the initiation stage, but amplifies the As 2 O 3 -mediated apoptotic program if it is persistently activated.

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“…Effects of autophagy and caspase inhibitors on the cytotoxicity of CrTX It has been reported that LDH leakage not only occurs during necrosis, but also during the process of apoptosis [28,29] . Since 3-MA interferes with the MTT assay, LDH leakage was measured as an index of cell death after co-treatment with CrTX and the autophagic inhibitors 3-MA (10 mmol/L) and NH 4 Cl (10 mmol/L).…”

Section: Vesicular Accumulation Of MDC After Crtx Treatmentmentioning

confidence: 99%

Autophagy is involved in cytotoxic effects of crotoxin in human breast cancer cell line MCF-7 cells

Yan

Yang

Qin

et al. 2007

Acta Pharmacologica Sinica

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Aim: To investigate the role of crotoxin (CrTX)‐induced autophagy in the death of MCF‐7 cells, a caspase‐3‐deficient, human breast cancer cell line. Methods: Cultured MCF‐7 cells were treated with various doses of CrTX, a phospholipase A2 (PLA2) isolated from the venom of the South American rattlesnake, Crotalus durissus terrificus. The cytotoxicity of CrTX in the presence and absence of caspase inhibitors was measured with methyl thiazolyl tetrazolium (MTT) and lactate dehydrogenase (LDH) leakage assays. The activation of autophagy was determined with transmission electron microscope and monodansylcadaverin (MDC) labeling. The upregulation of lysosomal enzymes, the release of cyto‐chrome c (cyto‐c), and the nuclear translocation of the apoptosis inducing factor (AIF) were examined by immunoblotting and immunofluorescence. Results: CrTX inhibited the viability of MCF‐7 cells in a dose‐ and time‐dependent manner. CrTX‐activated autophagy was revealed by punctuate MDC labeling, and an increase in the formation of autophagosomes as well as apoptosis, as evidenced by nuclear condensation and fragmentation. The activation of cathepsin B, D, and L, in addition to the release of cytochrome c and the relocation of AIF into nuclei, were observed after CrTX treatment. Autophagy inhibitors 3‐methyladenine (3‐MA), NH4Cl, and the pan‐caspase inhibitor, Z‐Val‐Ala‐Asp‐fluoromethylketone (Z‐Vad‐fmk), attenuated CrTX‐induced cell death. Conclusion: An autophagic mechanism contributes to the apoptosis of MCF‐7 cells induced by CrTX.

show abstract

NMDA-sensitive neurons profoundly influence delayed staurosporine-induced apoptosis in rat mixed cortical neuronal cultures

Cited by 15 publications

References 28 publications

In vitro and in vivo neuroprotective effect and mechanisms of glabridin, a major active isoflavan from Glycyrrhiza glabra (licorice)

In vitro and in vivo neuroprotective effect and mechanisms of glabridin, a major active isoflavan from Glycyrrhiza glabra (licorice)

Dynamic effects of autophagy on arsenic trioxide-induced death of human leukemia cell line HL60 cells

Autophagy is involved in cytotoxic effects of crotoxin in human breast cancer cell line MCF-7 cells

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