• Fisheries and Aquatic Sciences
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• 제1권1호
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• pp.24-29
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• 1998

Effect of extracellular calcium in vitellogenin (VTG) production in response to estradiol-17 $\beta$ $(E_2,\;2\times10^{-6}M)$ was examined in primary hepatocyte culture of rainbow trout, Onchorhynchus mykiss. Total calcium in estrogenized sera significantly increased, compared with the control, while diffusible calcium was insignificant. However, diffusible calcium in the incubation medium with $E_2$ was significantly reduced, compared with the control. The uptake of extracellular calcium by cultured hepatocytes signifIcantly increased 90 min after $E_2$ addition. Moreover, the accumulation of intracellular calcium increased in the cultures with $E_2$, regardless of the calcium concentrations in the incubation media. In addition, $E_2-primed $ VTG production was significantly decreased by withdrawal of E_2$ from the incubation medium. Moreover, VTG production by $E_2-primed$ hepatocytes was reduced by removing calcium from the incubation medium with or without $E_2$. These results suggest that the entry of extracellular calcium into the cytoplasm is an important step for VTG production in primary hepatocyte cultures in rainbow trout.

• BMB Reports
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• 제43권10호
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• pp.656-663
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• 2010

Amyloid precursor protein (APP), which is critically involved in the pathogenesis of Alzheimer's disease (AD), is cleaved by gamma/epsilon-secretase activity and results in the generation of different lengths of the APP Intracellular C-terminal Domain (AICD). In spite of its small size and short half-life, AICD has become the focus of studies on AD pathogenesis. Recently, it was demonstrated that AICD binds to different intracellular binding partners ('adaptor protein'), which regulate its stability and cellular localization. In terms of choice of adaptor protein, phosphorylation seems to play an important role. AICD and its various adaptor proteins are thought to take part in various cellular events, including regulation of gene transcription, apoptosis, calcium signaling, growth factor, and $NF-{\kappa}B$ pathway activation, as well as the production, trafficking, and processing of APP, and the modulation of cytoskeletal dynamics. This review discusses the possible roles of AICD in the pathogenesis of neurodegenerative diseases including AD.

• Toxicological Research
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• 제22권4호
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• pp.397-402
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• 2006

Lipid mediator such as lysophosphatidic acid (LPA) plays an important role in inflammation and wound heating, has been recently reported to induce influx of extracellular calcium into erythrocytes. This elevation in intracellular calcium level may cause destruction of membrane asymmetry and procoagulant microvesicle formation. Thus, we investigated if the lipid mediator could induce microvesicle formation as a result of extracellular calcium influx in human erythrocytes. Treatment with lipid mediator to erythrocytes resulted in microvesicle generation In a concentration-, time-dependent manner. Microvesicles formed expressed procoagulant phosphatidylserine (PS) on their surface membrane significantly as well. LPA did not affect the band 3 phosphorylation which is involved in morphological change in erythrocytes. Pretreatment with suramin did not inhibit LPA-induced microvesicle generation, suggesting microvesicle generation was not receptor-dependent pathway. Depletion of intracellular ATP levels in erythrocytes was suggested to be one of the mechanism for these events.

• The Korean Journal of Physiology and Pharmacology
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• 제6권5호
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• pp.241-246
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• 2002

We studied the excitatory action of morphine on the responses of dorsal horn neuron to iontophoretic application of excitatory amino acid and C-fiber stimulation by using the in vivo electrophysiological technique in the rat. In 137 of the 232 wide dynamic range (WDR) neurons tested, iontophoretic application of morphine enhanced the WDR neuron responses to N-methyl-D-aspartate (NMDA), kainate, and graded electrical stimulation of C-fibers. Morphine did not have any excitatory effects on the responses of low threshold cells. Morphine-induced excitatory effect at low ejection current was naloxone-reversible and reversed to an inhibitory action at high ejection current. NMDA receptor, calcium channel and intracellular $Ca^{2+}$ antagonists strongly antagonized the morphine-induced excitatory effect. These results suggest that changes in intracellular ionic concentration, especially $Ca^{2+},$ play an important role in the induction of excitatory effect of morphine in the rat dorsal horn neurons.

• 생약학회지
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• 제50권3호
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• pp.175-184
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• 2019

Mast cells are crucial as effector cells in the immediate-type allergic reaction. Lentinus edodes has been the popular edible mushroom in oriental countries and reported to have immunomodulatory, anti-tumor, anti-atherogenic, anti-viral, and anti-allergic activities. However, the roles of L. edodes in mast cell-mediated anaphylactic reaction have not been fully elucidated. In this research, we have demonstrated the effects of the methanol extract of L. edodes (MELE) on mast cell-mediated anaphylaxis-like and anaphylactic reactions. MELE suppressed systemic anaphylaxis-like reaction, plasma histamine levels, and ear swelling response in mice treated with compound 48/80. MELE also suppressed passive systemic and cutaneous anaphylaxis mediated by anti-dinitrophenyl IgE. In accordance with these findings, MELE dose-dependently decreased histamine release from RPMC evoked by compound 48/80 or the antigen-antibody reaction. To clarify the mechanism of degranulation system, intracellular cAMP levels as well as calcium influx in RPMC was evaluated. In compound 48/80-treated RPMC, MELE blocked calcium uptake into the cells. In addition, MELE elevated the intracellular cAMP content and significantly attenuated compound 48/80-induced cAMP reduction in RPMC. Taken together, we propose the clinical use of MELE in mast cell-mediated immediate-type allergic diseases.

• 한국전자현미경학회:학술대회논문집
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• 한국현미경학회 1993년도 제24회 학술대회 연제 초록
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• pp.13-13
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• 1993

• Journal of Plant Biology
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• 제38권3호
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• pp.243-250
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• 1995

Involvement of calcium in signal transduction of salt stress was investigated in 1.7 M NaCl adapted Dunaliella salina, extremely halotolerant, unicellular green alga. When hyperosmotic (3.4 M NaCl) or Hypoosmotic (0.8 M NaCl) stress was treated, extracellular calcium was influxed in or intracellular calcium effluxed from D. salina, respectively, and these fluxes were proportional to the degree of stress. This might indicate indirectly that the change of calcium level occurred within the cells. In addition, the change of calcium flux was ahead of glycerol synthesis which has been known as the physiological response to salt stress. Osmoregulation was affected byextracellular calcium concentration, and increase of glycerol content as an osmoticum was inhibited about 50% by treatment of TFP and W-7 known as calmodulin specific inhibitors. Furthermore, in the case of the hyperosmotic stressed cells, the amount of 21 kD and 39 kD protein appeared to be calcium binding protein were increased. Among these, the 39 kD protein was detected only in the hyperosmotic stressed cells. The results obtained in the present work suggest that the possibility of calcium as a second messenger in the transduction of salt stress signal exists in the osmoregulation system of D. salina.

• The Korean Journal of Physiology and Pharmacology
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• 제21권2호
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• pp.233-239
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• 2017

Intracellular calcium ($Ca^{2+}$) oscillation is an initial event in digestive enzyme secretion of pancreatic acinar cells. Reactive oxygen species are known to be associated with a variety of oxidative stress-induced cellular disorders including pancreatitis. In this study, we investigated the effect of hydrogen peroxide ($H_2O_2$) on intracellular $Ca^{2+}$ accumulation in mouse pancreatic acinar cells. Perfusion of $H_2O_2$ at $300{\mu}M$ resulted in additional elevation of intracellular $Ca^{2+}$ levels and termination of oscillatory $Ca^{2+}$ signals induced by carbamylcholine (CCh) in the presence of normal extracellular $Ca^{2+}$. Antioxidants, catalase or DTT, completely prevented $H_2O_2$-induced additional $Ca^{2+}$ increase and termination of $Ca^{2+}$ oscillation. In $Ca^{2+}$-free medium, $H_2O_2$ still enhanced CCh-induced intracellular $Ca^{2+}$ levels and thapsigargin (TG) mimicked $H_2O_2$-induced cytosolic $Ca^{2+}$ increase. Furthermore, $H_2O_2$-induced elevation of intracellular $Ca^{2+}$ levels was abolished under sarco/endoplasmic reticulum $Ca^{2+}$ ATPase-inactivated condition by TG pretreatment with CCh. $H_2O_2$ at $300{\mu}M$ failed to affect store-operated $Ca^{2+}$ entry or $Ca^{2+}$ extrusion through plasma membrane. Additionally, ruthenium red, a mitochondrial $Ca^{2+}$ uniporter blocker, failed to attenuate $H_2O_2$-induced intracellular $Ca^{2+}$ elevation. These results provide evidence that excessive generation of $H_2O_2$ in pathological conditions could accumulate intracellular $Ca^{2+}$ by attenuating refilling of internal $Ca^{2+}$ stores rather than by inhibiting $Ca^{2+}$ extrusion to extracellular fluid or enhancing $Ca^{2+}$ mobilization from extracellular medium in mouse pancreatic acinar cells.

• The Korean Journal of Physiology and Pharmacology
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• 제2권2호
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• pp.173-184
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• 1998

The present study was undertaken to examine the influence of glucocorticoids on the secretory responses of catecholamines (CA) evoked by acetylcholine (ACh), DMPP, McN-A-343, excess K^+$ and Bay-K-8644 from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. The perfusion of the synthetic glucocorticoid dexamethasone (10-100\;{\mu}M$) into an adrenal vein for 20 min produced a dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM), excess K^+$ (a membrane-depolarizor 56 mM), DMPP (a selective nicotinic receptor agonist, 100\;{\mu}M$ for 2 min), McN-A-343 (a muscarinic receptor agonist, 100\;{\mu}M$ for 4 min), Bay-K-8644 (a calcium channel activator, 10\;{\mu}M$ for 4 min) and cyclopiazonic acid (a releaser of intracellular $Ca^{2+}$, 10\;{\mu}M$ for 4 min). Similarly, the preperfusion of hydrocortisone (30\;{\mu}M$) for 20 min also attenuated significantly the secretory responses of CA evoked by nicotinic and muscarinic receptor stimulation as well as membrane-depolarization, $Ca^{2+}$ channel activation and the release of intracellular $Ca^{2+}$. Furthermore, even in the presence of betamethasone (30{\mu}M$), CA secretion evoked by ACh, excess K^+$, DMPP and McN-A-343 was also markedly inhibited. Taken together, the present results suggest that glucocorticoids cause the marked inhibition of CA secretion evoked by both cholinergic nicotinic and muscarinic receptor stimulation from the isolated perfused rat adrenal gland, indicating strongly that this inhibitory effect may be mediated by inhibiting influx of extracellular calcium as well as the release of intracellular calcium in the rat adrenomedullary chromaffin cells.

• The Korean Journal of Physiology and Pharmacology
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• 제21권1호
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• pp.55-64
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• 2017

Progressive memory impairment such as that associated with depression, stroke, and Alzheimer's disease (AD) can interfere with daily life. In particular, AD, which is a progressive neurodegenerative disorder, prominently features a memory and learning impairment that is related to changes in acetylcholine and abnormal ${\beta}$-amyloid ($A{\beta}$) deposition in the brain. In the present study, we investigated the effects of dehydroevodiamine HCl (DHED) on cognitive improvement and the related mechanism in memory-impaired rat models, namely, a scopolamine-induced amnesia model and a $A{\beta}_{1-42}$-infused model. The cognitive effects of DHED were measured using a water maze test and a passive avoidance test in the memory-impaired rat models. The results demonstrate that DHED (10 mg/kg, p.o.) and Donepezil (1 mg/kg, p.o.) ameliorated the spatial memory impairment in the scopolamine-induced amnestic rats. Moreover, DHED significantly improved learning and memory in the $A{\beta}_{1-42}$-infused rat model. Furthermore, the mechanism of these behavioral effects of DHED was investigated using a cell viability assay, reactive oxygen species (ROS) measurement, and intracellular calcium measurement in primary cortical neurons. DHED reduced neurotoxicity and the production of $A{\beta}$-induced ROS in primary cortical neurons. In addition, similar to the effect of MK801, DHED decreased intracellular calcium levels in primary cortical neurons. Our results suggest that DHED has strong protective effects against cognitive impairments through its antioxidant activity and inhibition of neurotoxicity and intracellular calcium. Thus, DHED may be an important therapeutic agent for memory-impaired symptoms.