Calcium and reactive oxygen species mediate staurosporine-induced mitochondrial dysfunction and apoptosis in PC12 cells

Kruman, Inna I.; Guo, Qing; Mattson, Mark P.

doi:10.1002/(sici)1097-4547(19980201)51:3<293::aid-jnr3>3.0.co;2-b

Cited by 361 publications

(253 citation statements)

References 93 publications

(102 reference statements)

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“…First, ROS are produced in the process of apoptotic cell death (Hockenbery et al, 1993;Bredesen, 1994;Prehn et al, 1997;Krohn et al, 1998). Second, ROS scavengers prevent apoptosis (Hockenbery et al, 1993;Troy and Shelanski, 1994;Greenlund et al, 1995;Kruman et al, 1998). Third, exposure to pro-oxidants can induce apoptosis (Ratan et al, 1994;Whittemore et al, 1995).…”

Section: Metabolism Of Arachidonic Acidmentioning

confidence: 99%

Cellular and Molecular Pathways of Ischemic Neuronal Death

Won¹,

Kim²,

Gwag³

2002

BMB Reports

201

172

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Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of Ca 2+ and Na + that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

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Section: Metabolism Of Arachidonic Acidmentioning

confidence: 99%

Cellular and Molecular Pathways of Ischemic Neuronal Death

Won¹,

Kim²,

Gwag³

2002

BMB Reports

201

172

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“…It has been reported that elevation of the intracellular Ca 2+ level is regarded as an important mediator of apoptosis (8). Staurosporine treatment of PC12 cells resulted in both a rapid (min) and prolonged (h) elevation of intracellular Ca 2+ (9). The endoplasmic reticulum is a critical site responsible for the regulator of intracellular calcium homeostasis.…”

Section: Introductionmentioning

confidence: 99%

“…So, high level expression of CHOP and GRP78/ BiP can be recognized as biomarks of ER stress. Because ER stress leads to increase in cytosolic calcium levels (12) and Ca 2+ increase is associated with apoptosis signaling (9), it is an excellent strategy in chemotherapy that induce ER stress.…”

Section: Introductionmentioning

confidence: 99%

Tubeimoside-1 induces G2/M phase arrest and apoptosis in SKOV-3 cells through increase of intracellular Ca2+ and caspase-dependent signaling pathways

Yang

2011

Int J Oncol

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Abstract. Tubeimoside-1 (TBMS1) extracted from Bolbostemma paniculatum (Maxim), is a traditional Chinese herb with anticancer potential. It induces apoptosis in a number of human carcinoma cell lines, but the mechanism has remained unclear.In the present study, we investigated the pro-apoptotic activity of TBMS1 against SKOV-3 cell lines and the underlying mechanisms. Treatment with TBMS1 resulted in dose-and time-dependent inhibition of proliferation, led to arrest in phase G 2 /M of the cell cycle and increased the levels of intracellular Ca 2+ . Furthermore, TBMS1 up-regulated the levels of the glucose-regulated protein 78/immunoglobuin heavy chain binding protein (GRP78/Bip), C/EBP homologous protein (CHOP), Bax, and cleaved caspase-3 and down-regulated the levels of Bcl-2. It was shown to be linked to activation of the extracellular signal-regulated kinase (ERK) 1 and 2 signal transduction pathway. A decrease in Bcl-2/Bax ratio with increased expression of caspase-3, and intracellular Ca 2+ provide compelling evidence that TBMS1-induced apoptosis is mediated by the mitochondrial pathway. The results of the present study suggest that TBMS1 has immense potential in cancer prevention and therapy based on its antiproliferative and apoptosis inducing effects.

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“…Staurosporine, a potent protein kinase C inhibitor with a broad spectrum of activity [36], is known to induce apoptosis [37,43] and to cause OS through mitochondrially generated ROS in a variety of cells [20]. Under normal conditions, ROS-induced damage is kept in check by an efficient array of cell antioxidant systems, whereas under pathological conditions, the oxidant/antioxidant balance is altered, either primarily or secondarily.…”

Section: Discussionmentioning

confidence: 99%

Study of the cytotoxicity and antioxidant capacity of N/OFQ(1–13)NH2 and its structural analogues

Kirkova

Zamfirova

Leśkiewicz

et al. 2009

Pharmacological Reports

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Abstract:The effect of side-chain shortening of N/OFQ(1-13)NH 2 at position 9 ([Orn 9 ]N/OFQ(1-13)NH 2 , [Dab 9 ]N/OFQ(1-13)NH 2 , [Dap 9 ]N/OFQ(1-13)NH 2 ) was studied regarding potential toxicity and antioxidant capacity. Staurosporine-and H 2 O 2 -induced damage of SH-SY5Y neuroblastoma cells was not changed in the presence of N/OFQ(1-13)NH 2 and [Orn 9 ]N/OFQ(1-13)NH 2 , but was strongly enhanced in the presence of [Dab 9 ]N/OFQ(1-13)NH 2 and [Dap 9 ]N/OFQ(1-13)NH 2 . Moreover, treatment of cells with the latter two analogues alone led to cell injury. Neuropeptide-dependent differences in the viability of SH-SY5Y cells were also observed, i.e., a cytoprotective effect was observed only in the presence of N/OFQ(1-13)NH 2 and [Orn 9 ]N/OFQ(1-13)NH 2 . Compared to [Dab 9 ]N/OFQ(1-13)NH 2 and [Dap 9 ]N/OFQ(1-13)NH 2 , the effects of N/OFQ(1-13)NH 2 and [Orn 9 ]N/OFQ(1-13)NH 2 were more beneficial in systems generating free oxygen radicals (O 2 -and . OH), as well as on the antioxidant status of rat brain and liver. Taken together, our findings show that N/OFQ(1-13)NH 2 and its structural analogue [Orn 9 ]N/OFQ(1-13)NH 2 possess more favorable profiles than the other two nociceptin (N/OFQ) analogues. The present results suggest that shortening of the side-chain of N/OFQ(1-13)NH 2 might increase cell damage and reduce the viability of SH-SY5Y neuroblastoma cells. Moreover, such alterations may lead to changes in free-oxygen generating systems and in antioxidant status in animal tissues.

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Calcium and reactive oxygen species mediate staurosporine-induced mitochondrial dysfunction and apoptosis in PC12 cells

Cited by 361 publications

References 93 publications

Cellular and Molecular Pathways of Ischemic Neuronal Death

Cellular and Molecular Pathways of Ischemic Neuronal Death

Tubeimoside-1 induces G2/M phase arrest and apoptosis in SKOV-3 cells through increase of intracellular Ca2+ and caspase-dependent signaling pathways

Study of the cytotoxicity and antioxidant capacity of N/OFQ(1–13)NH2 and its structural analogues

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