Ionomycin-induced calcium influx induces neurite degeneration in mouse neuroblastoma cells: analysis of a time-lapse live cell imaging system

Nakamura, Saki; Nakanishi, Ayumi; Takazawa, Minami; Okihiro, Shunsuke; Urano, Shiro; Fukui, Koji

doi:10.1080/10715762.2016.1227074

Cited by 18 publications

(16 citation statements)

References 53 publications

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“…ROS formation causes lipid peroxidation 29 . We monitored possible lipid peroxidation using two fluorescence sensors, MitoPeDPP 30 and BODIPY 581/591 C11 31 . Both sensors detected lipid peroxidation in DDHD2 KO MEFs (Supplementary Figures 6a and b).…”

Section: Resultsmentioning

confidence: 99%

Loss of DDHD2, whose mutation causes spastic paraplegia, promotes reactive oxygen species generation and apoptosis

Maruyama¹,

Baba²,

Maemoto³

et al. 2018

Cell Death Dis

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DDHD2/KIAA0725p is a mammalian intracellular phospholipase A1 that exhibits phospholipase and lipase activities. Mutation of the DDHD2 gene causes hereditary spastic paraplegia (SPG54), an inherited neurological disorder characterized by lower limb spasticity and weakness. Although previous studies demonstrated lipid droplet accumulation in the brains of SPG54 patients and DDHD2 knockout mice, the cause of SPG54 remains elusive. Here, we show that ablation of DDHD2 in mice induces age-dependent apoptosis of motor neurons in the spinal cord. In vitro, motor neurons and embryonic fibroblasts from DDHD2 knockout mice fail to survive and are susceptible to apoptotic stimuli. Chemical and probe-based analysis revealed a substantial decrease in cardiolipin content and an increase in reactive oxygen species generation in DDHD2 knockout cells. Reactive oxygen species production in DDHD2 knockout cells was reversed by the expression of wild-type DDHD2, but not by an active-site DDHD2 mutant, DDHD2 mutants related to hereditary spastic paraplegia, or DDHD1, another member of the intracellular phospholipase A1 family whose mutation also causes spastic paraplegia (SPG28). Our results demonstrate the protective role of DDHD2 for mitochondrial integrity and provide a clue to the pathogenic mechanism of SPG54.

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Section: Resultsmentioning

confidence: 99%

Loss of DDHD2, whose mutation causes spastic paraplegia, promotes reactive oxygen species generation and apoptosis

Maruyama¹,

Baba²,

Maemoto³

et al. 2018

Cell Death Dis

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show abstract

“…(35) In contrast to our results, Kleinridders et al (38) reported that mitochondrial dysfunction is induced by downregulation of HSP60 in diabetic mice, and ROS production and insulin resistance are increased. In our previous study, we found that mitochondria accumulate in neurite beading regions (18) and induce superoxide production in hydrogen peroxide-treated neuronal cells. (39) Mitochondria play crucial roles in the branching and elongation of neurites.…”

Section: Discussionmentioning

confidence: 98%

“…(16,17) However, neurites can expand and contract easily by external stimuli such as changes in pH, ionic composition, etc. (18,19) Furthermore, we have found that treatment with a low concentrations of hydrogen peroxide induces neurite degeneration prior to cell death. (8,9) It is well known that neurite degeneration starts from the distal end of neurites in Wallerian Degeneration Slow ( WLD s ) models.…”

Section: Discussionmentioning

confidence: 98%

Proteomic study on neurite responses to oxidative stress: search for differentially expressed proteins in isolated neurites of N1E-115 cells

Fukui

Okihiro

Ohfuchi

et al. 2019

J. Clin. Biochem. Nutr.

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Reactive oxygen species attack several living organs and induce cell death. Previously, we found axonal/dendrite degeneration before the induction of cell death in hydrogen peroxide treated neuro blastoma: N1E 115 cells and primary neurons. This phenomenon may be connected with membrane oxidation, microtubule desta bilization and disruption of intracellular calcium homeostasis. However, its detailed mechanisms are not fully understood. Here, we identified proteins after treatment with hydrogen peroxide using isolated neurites by liquid chromatography matrix assisted laser desorption/ionization time of flight/time of flight analysis. Twenty one proteins were increased after treatment with hydro gen peroxide. Specifically, 5 proteins which were secretogranin 1, heat shock protein family D member 1, Brain acid soluble protein 1, heat shock 70 kDa protein 5 and superoxide dismutase 1, were identified of all experiments and increased in isolated neurites of hydrogen peroxide treated cells compared to the controls. Further more, secretogranin 1 and heat shock protein family D member 1 protein expressions were significantly increased in normal aged and Alzheimer's transgenic mice brains. These results indicate that secretogranin 1 and heat shock protein family D member 1 might contribute to reactive oxygen species induced neurite degeneration. Both proteins have been related to neurodegenerative disorders, so their study may shed light on neurite dysfunction.

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“…LPO was determined using MitoPeDPP [13]. Cells were washed twice with PBS, and then treated with 0.5 µM MitoPeDPP in Hanks' HEPES buffer for 15 min at 37°C under dark conditions.…”

Section: Sirna and Transfectionmentioning

confidence: 99%

Romidepsin and Tamoxifen Cooperatively Induce Senescence of Pancreatic Cancer Cells Through Downregulation of FOXM1 Expression and Induction of ROS/Lipid Peroxidation

Okuma

Honma

Urano

et al. 2021

Preprint

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Although progress has been made in chemotherapeutic strategies against pancreatic cancer, overall survival has not significantly improved over the past decade. Thus, the development of better therapeutic regimens remains a high priority. Pancreatic cancer cell lines were treated with romidepsin, an inhibitor of histone deacetylase, and tamoxifen, and their effects on cell growth, signaling and gene expression were determined. Xenografts of human pancreatic cancer CFPAC1 cells were treated with romidepsin and tamoxifen to determine their effects on tumor growth. The inhibition of the growth of pancreatic cancer cells induced by romidepsin and tamoxifen was effectively reduced by N-acetyl cysteine and α-tocopherol, respectively. The combined treatment greatly induced reactive oxygen species production and mitochondrial lipid peroxidation, and these effects were prevented by N-acetyl cysteine and α-tocopherol. Tamoxifen enhanced romidepsin-induced cell senescence. FOXM1 expression was markedly downregulated in pancreatic cancer cells treated with romidepsin, and tamoxifen further reduced FOXM1 expression in cells treated with romidepsin. Siomycin A, an inhibitor of FOXM1, induced senescence in pancreatic cancer cells. Similar results were obtained in knockdown of FOXM1 expression by siRNA. Since FOXM1 is used as a prognostic marker and therapeutic target for pancreatic cancer, a combination of the clinically available drugs romidepsin and tamoxifen might be considered for the treatment of patients with pancreatic cancer.

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Ionomycin-induced calcium influx induces neurite degeneration in mouse neuroblastoma cells: analysis of a time-lapse live cell imaging system

Cited by 18 publications

References 53 publications

Loss of DDHD2, whose mutation causes spastic paraplegia, promotes reactive oxygen species generation and apoptosis

Loss of DDHD2, whose mutation causes spastic paraplegia, promotes reactive oxygen species generation and apoptosis

Proteomic study on neurite responses to oxidative stress: search for differentially expressed proteins in isolated neurites of N1E-115 cells

Romidepsin and Tamoxifen Cooperatively Induce Senescence of Pancreatic Cancer Cells Through Downregulation of FOXM1 Expression and Induction of ROS/Lipid Peroxidation

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