Electric Pulse Stimulation Induces NMDA Glutamate Receptor mRNA in NIH3T3 Mouse Fibroblasts

Okutsu, Saeko; Hatakeyama, Hiroyasu; Kanazaki, Makoto; Tsubokawa, Hiroshi; Nagatomi, Ryoichi

doi:10.1620/tjem.215.181

Cited by 9 publications

(7 citation statements)

References 28 publications

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“…These various stressors may naturally induce membrane dysfunction, mitochondrial stress, and ER stress, and could activate the caspase pathway (38). Moreover, electric pulse treatment induces intracellular Ca 2+ flux (11,39). Accordingly, the primary mechanism underlying apoptosis in response to LVEPs may involve membrane structural change, vesicle formation, and disrupted ion transport, resulting in the influx of Ca 2+ and ONCOLOGY REPORTS 23: 1425-1433, 2010 Figure 6.…”

Section: Discussionmentioning

confidence: 99%

Activation of caspases and apoptosis in response to low-voltage electric pulses

Matsuki

Takeda²,

Ishikawa³

et al. 2010

Oncol Rep

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Abstract. Few studies have examined apoptosis induced by low-voltage electric pulses (LVEPs). LVEP-induce changes in membrane potential that are below the membrane breakdown threshold and increase membrane permeability without electroporation (pore formation) through the transport of extracellular substances via phagocytosis. We demonstrated that propidium iodide uptake and apoptosis increased in accordance with the duration and number of LVEPs in B16 cells, which showed relatively good viability under mild electric field conditions. We showed that LVEP-induced apoptosis was achieved through caspase-8 and -9 activation and subsequent caspase-3 activation. Long-duration LVEPs caused only mild cell damage, such that the apoptosis ratio (apoptosis/total cell death) in electric pulse-treated cells was similar to that in non-treated control cells. To assess the relative degree of caspase dependency in LVEP-induced apoptosis, the apoptosis rate and caspase-3 activity were analyzed using a pan-caspase inhibitor (Z-VAD-FMK). Z-VAD-FMK treatment inhibited, but did not abolish, LVEP-induced apoptosis, indicating that caspases other than caspase-3 participate in this pathway. Moreover, LVEP treatment inhibited cell growth, suggesting that LVEP treatment may be a valuable anticancer therapy. Although the mechanism of LVEP-induced apoptosis remains unclear, it may be related to dysfunctional membrane transport of Ca 2+ and other extracellular substances involved in caspase activation.

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Section: Discussionmentioning

confidence: 99%

Activation of caspases and apoptosis in response to low-voltage electric pulses

Matsuki

Takeda²,

Ishikawa³

et al. 2010

Oncol Rep

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“…Early structure-activity studies have established that the structure of glutamate is ideal for the activation of NMDARs. In the last few years, NMDA-type glutamate receptors have been detected in fibroblasts, including human fibroblast-like synoviocytes [ 25 ], NIH3T3 mouse fibroblasts [ 26 ], and human periodontal ligament fibroblasts [ 27 ]. In our previous report demonstrating the abundant release of glutamate in hyperoxia-induced acute lung injury in newborn rats [ 3 ], our data suggested that lung fibroblasts may be excited by endogenous glutamate via NMDAR activation.…”

Section: Introductionmentioning

confidence: 99%

N-methyl-D-aspartate receptor activation mediates lung fibroblast proliferation and differentiation in hyperoxia-induced chronic lung disease in newborn rats

et al. 2016

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BackgroundPrevious studies have suggested that endogenous glutamate and its N-methyl-D-aspartate receptors (NMDARs) play important roles in hyperoxia-induced acute lung injury in newborn rats. We hypothesized that NMDAR activation also participates in the development of chronic lung injury after withdrawal of hyperoxic conditions.MethodsIn order to rule out the anti-inflammatory effects of NMDAR inhibitor on acute lung injury, the efficacy of MK-801 was evaluated in vivo using newborn Sprague-Dawley rats treated starting 4 days after cessation of hyperoxia exposure (on postnatal day 8). The role of NMDAR activation in hyperoxia-induced lung fibroblast proliferation and differentiation was examined in vitro using primary cells derived from the lungs of 8-day-old Sprague-Dawley rats exposed to hyperoxic conditions.ResultsHyperoxia for 3 days induced acute lung injury in newborn rats. The acute injury almost completely disappeared 4 days after cessation of hyperoxia exposure. However, pulmonary fibrosis, impaired alveolarization, and decreased pulmonary compliance were observed on postnatal days 15 and 22. MK-801 treatment during the recovery period was found to alleviate the chronic damage induced by hyperoxia. Four NMDAR 2 s were found to be upregulated in the lung fibroblasts of newborn rats exposed to hyperoxia. In addition, the proliferation and upregulation of alpha-smooth muscle actin and (pro) collagen I in lung fibroblasts were detected in hyperoxia-exposed rats. MK-801 inhibited these changes.ConclusionsNMDAR activation mediated lung fibroblast proliferation and differentiation and played a role in the development of hyperoxia-induced chronic lung damage in newborn rats.

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“…We then examined whether the BMAA-mediated suppression of the G1/S transition required activation of glutamate receptors, given that NIH3T3 cells may express glutamate receptors, including NMDA glutamate receptors 28 , and that the concentrations of BMAA (1 and 3 mM) used in the present study were previously shown to induce excitotoxicity in neurons through NMDA glutamate receptor activation 7,19 . The excitotoxicity of BMAA is known to be strongly dependent on bicarbonate as a cofactor 7,19 .…”

Section: Resultsmentioning

confidence: 99%

β-N-methylamino-L-alanine (BMAA) suppresses cell cycle progression of non-neuronal cells

Okamoto

Esumi

Hamaguchi-Hamada

et al. 2018

Sci Rep

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β-N-methylamino-L-alanine (BMAA), a natural non-proteinaceous amino acid, is a neurotoxin produced by a wide range of cyanobacteria living in various environments. BMAA is a candidate environmental risk factor for neurodegenerative diseases such as amyotrophic lateral sclerosis and Parkinson-dementia complex. Although BMAA is known to exhibit weak neuronal excitotoxicity via glutamate receptors, the underlying mechanism of toxicity has yet to be fully elucidated. To examine the glutamate receptor-independent toxicity of BMAA, we investigated the effects of BMAA in non-neuronal cell lines. BMAA potently suppressed the cell cycle progression of NIH3T3 cells at the G1/S checkpoint without inducing plasma membrane damage, apoptosis, or overproduction of reactive oxygen species, which were previously reported for neurons and neuroblastoma cells treated with BMAA. We found no evidence that activation of glutamate receptors was involved in the suppression of the G1/S transition by BMAA. Our results indicate that BMAA affects cellular functions, such as the division of non-neuronal cells, through glutamate receptor-independent mechanisms.

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Electric Pulse Stimulation Induces NMDA Glutamate Receptor mRNA in NIH3T3 Mouse Fibroblasts

Cited by 9 publications

References 28 publications

Activation of caspases and apoptosis in response to low-voltage electric pulses

Activation of caspases and apoptosis in response to low-voltage electric pulses

N-methyl-D-aspartate receptor activation mediates lung fibroblast proliferation and differentiation in hyperoxia-induced chronic lung disease in newborn rats

β-N-methylamino-L-alanine (BMAA) suppresses cell cycle progression of non-neuronal cells

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