• YAKHAK HOEJI
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• v.45 no.3
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• pp.282-286
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• 2001

To investigate the different mechanism between ATP and compound 48/80 (C$_{48}$80/)-induced histamine release, we observed effects of calcium antagonists in histamine release of rat peritoneal mast cells. Verapamil and diltiazem (voltage-dependent calcium channel blocker) and TMB-8 (a blocker of intracellular calcium release) significantly inhibited ATP-induced histamine release, but did not inhibit $C_{48}$80/-induced histamine release. Econazole (a blocker of receptor-operated calcium channel) dose-dependently inhibited both ATP and $C_{48}$80/-induced histamine release, but inhibitory effect of econazole in ATP-induced histamine release was more potent than that in $C_{48}$80/-induced histamine. EGTA dose-dependently inhibited ATP and $C_{48}$80/-induced histamine release, but $C_{48}$80/-induced histamine release was slightly inhibited by high concentrations (>2 mM) of EGTA. These results suggest that ATP-induced histamine release is related to broth intracellular calcium release and extracellular calcium influx via voltage-dependent calcium channel and receptor-operated calcium channel. $C_{48}$80/-induced histamine release is related to extracellular calcium influx, especially by receptor-operated calcium channel rather than voltage-dependent calcium channel.

• Archives of Pharmacal Research
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• v.22 no.2
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• pp.119-123
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• 1999

Parathyroid hormone (PTH) treatment of bone and kidney-derived cells not only activates adenyly cyclase buy also increases intracellular free calcium, and translocates protein kinase C (PKC) from cytosol to plasma membranes. We have found that acute phorbol ester pretreatment significantly decreases PTH-induced calcium transients and the effect of phorbol ester was antagonized by staurosporine (ST). Although the major effect of ST in that study was the reversal of the action of phorbol ester, it appeared that ST may also have promoted the effect of PTH directly. To further investigate the observation, we examined the effect of ST on the intracellular calcium transients induced by PTH and $\alpha$-thrombin ($\alpha$-TH). For calcium transient experiments, UMR-106 cells were loaded with 2 mM fluo-acetoxymethylester for 30 min at room temperature. The cells were then washed and suspended in buffer containing 1 mM calcium. Fluorescence was detected at 530 nm, with excitation at 505 nm. ST alone did not cause calcium transients, but enhanced the transients elicited by PTH response. added 5 min before the hormone. Another protein kinase inhibitor H-7 likewise enhanced the calcium responses elicited by PTH, while genistein did not affect PTH response. Calcium transients elicited by $\alpha$-TH were also enhanced by ST. The results suggest that there might be tonically activated endogenous protein kinase(s) which inhibit calcium signaling of some calcemic agents.

• BMB Reports
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• v.28 no.5
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• pp.392-397
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• 1995

The effect of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on the intracellular $Ca^{2+}$ level was studied in NIH3T3 fibroblast cells. A reduction of the intracellular $Ca^{2+}$ level was observed after exposure to 300 ${\mu}m$ MNNG. However, the intracellular level of $IP_3$, a well-known regulator of $Ca^{2+}$ release from internal storage, was not changed by MNNG treatment. Instead, a reduction of the intracellular NAD level was observed. NAD as well as $IP_3$ stimulated intracellular $Ca^{2+}$ release from permeabilized cells. The treatment of 3-aminobenzamide, which inhibited the MNNG-induced reduction of the NAD level, also prevented the MNNG-induced decrease of the $Ca^{2+}$ level. Our data suggest that MNNG reduces the intracellular $Ca^{2+}$ level by NAD depletion in NIH3T3 cells.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.615-621
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• 1999

In spite many evidences has supported the cardioprotective effect of bradykinin, its direct effects at the cell level are still under question. We investigated the both effects of bradykinin (BK) on $Ca^{2+}-related$ ionic currents using whole cell voltage clamp technique in rabbit cardiomyocytes and on the intracellular $Ca^{2+}$ transient using calcium sensitive fluorescence dye, indo-1AM. Simultaneously with recording intracellular $Ca^{2+}$ transients, cell contractility was estimated from the changes in length of the electrical stimulated rat cardiac myocytes. L-type $Ca^{2+}$ current decreased by bradykinin at the entire voltage range. Inward tail current increased initially up to its maximum about 4 min after exposing myocytes to BK, and then gradually decreased again by further exposure to BK. This tail current decreased remarkably at washing BK off but slowly recovered ca. 20 min later. The change in cell contractility was similar to that in tail current showing initial increase followed by gradual decrease. Removal of BK brought remarkable decrease in contractility, which was recovered $15{\sim}20$ min after cessation of electrical stimulation. Bradykinin increased $Ca^{2+}$ transient initially but after some time $Ca^{2+}$ transient also decreased coincidentally with contractility. From these results, it is suggested that bradykinin exerts directly its cardioprotective effect on the single myocytes by decreasing the intracellular $Ca^{2+}$ level followed by an initial increase in $Ca^{2+}$ transient.

• The Korean Journal of Food And Nutrition
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• v.35 no.6
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• pp.531-536
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• 2022

Umami taste-yielding foods, such as, Joseonganjang, dried anchovies, dried shiitake, dried Konbu (kelp), and Yukjeot, are widely used in the Korean cuisine as soup base. While Umami taste enhancement related to Kokumi taste substances has been proposed in human sensory studies, the potential action of Kokumi taste substances has not been explored on calcium-sensing receptors (CaSR), here referred to as Kokumi taste receptors. In this study, we investigated the effect of Umami taste-yielding foods on Kokumi taste receptors using cells expressing human CaSR. We monitored the temporal changes in intracellular Ca²⁺ in HEK293T cells expressing CaSR in response to aqueous extract of Joseonganjang, dried anchovies, dried shiitake, dried Konbu, and Yukjeot. Kokumi substances tested-glutathione and γ-Glu-Val-Gly- evoked intracellular Ca²⁺ influx in a concentration-dependent manner. A similar increment of intracellular Ca²⁺ influx was induced by Joseonganjang, Yukjeot, and dried anchovies, but not by dried shiitake and dried Konbu. Only Joseonganjang- and Yukjeot-evoked intracellular Ca²⁺ influx was significantly reduced by NPS 2143, a CaSR-specific antagonist. These data indicated that some Umami substances/Umami-yielding materials could activate CaSR, but this property was not observed for all the Umami tasting substances.

• Biomedical Science Letters
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• v.12 no.1
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• pp.9-16
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• 2006

We investigated the effects of 835-MHz electromagnetic field (EMF), one of the most popular communication frequency band in Korean code-division multiple-access (CDMA) mobile phone system, on cellular signal transduction. For this, we examined the change of intracellular calcium $([Ca^{2+}]_i)$, reactive oxygen species (ROS) and F-actin polymerization after exposure to 835-MHz EMF followed by the treatment of agonists in Rat-2 fibroblast cells. Culture cells were pretreated with serum-tree medium and concomitantly exposed to 835-MHz at specific absorption rate (SAR) of 4.0 W/kg for 24 hr in a specialized designed apparatus based on Transverse Electro Magnetics (TEM) wave theory. Intracellular $Ca^{2+}$ responses to lysophosphatidic acid (LPA) and epidermal growth factor (EGF) in Rat-2 fibroblast after exposure to 835-MHz EMF were shown to be similar pattern as observed in normal cultured cells. However, the LPA-induced calcium spiking was slightly delayed to 7 sec and sustained thereafter to a little higher ground level under 835-MHz EMF radiation compared to unexposed cells. ROS production level by LPA in the exposed cells was not different from that in control. Furthermore, LPA induced the production of stress fibers with no significant difference in the exposed and unexposed cells. These results suggest that mobile phone radiation (835-MHz, SAR 4.0 W/kg) may not be directly related to signal transduction in Rat-2 fibroblasts except the slight effect of calcium spiking in LPA-induced cells but remain to be further elucidated for possible indirect intervention.

• International Journal of Oral Biology
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• v.38 no.1
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• pp.5-12
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• 2013

Recent studies indicate that reactive oxygen species (ROS) can act as modulators of neuronal activity, and are critically involved in persistent pain primarily through spinal mechanisms. In this study, we investigated the effects of NaOCl, a ROS donor, on neuronal excitability and the intracellular calcium concentration ($[Ca^{2+}]_i$) in spinal substantia gelatinosa (SG) neurons. In current clamp conditions, the application of NaOCl caused a membrane depolarization, which was inhibited by pretreatment with phenyl-N-tert-buthylnitrone (PBN), a ROS scavenger. The NaOCl-induced depolarization was not blocked however by pretreatment with dithiothreitol, a sulfhydryl-reducing agent. Confocal scanning laser microscopy was used to confirm whether NaOCl increases the intracellular ROS level. ROS-induced fluorescence intensity was found to be increased during perfusion of NaOCl after the loading of 2',7'-dichlorofluorescin diacetate ($H_2DCF$-DA). NaOCl-induced depolarization was not blocked by pretreatment with external $Ca^{2+}$ free solution or by the addition of nifedifine. However, when slices were pretreated with the $Ca^{2+}$ ATPase inhibitor thapsigargin, NaOCl failed to induce membrane depolarization. In a calcium imaging technique using the $Ca^{2+}$-sensitive fluorescence dye fura-2, the $[Ca^{2+}]_i$ was found to be increased by NaOCl. These results indicate that NaOCl activates the excitability of SG neurons via the modulation of the intracellular calcium concentration, and suggest that ROS induces nociception through a central sensitization.

• Biomolecules & Therapeutics
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• v.19 no.2
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• pp.181-186
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• 2011

Beta-amyloid (A${\beta}$) is considered as one of the major causes of Alzheimer's disease. This study examined the neuroprotective effects of chlorogenic acid, a naturally occurring polyphenol which is distributed widely in plants, fruits and vegetables, against A${\beta}$-induced toxicity. A${\beta}$ decreased significantly the viability of PC12 cells. This was accompanied by an increase in the intracellular calcium levels and cleaved caspase-3. In addition, A${\beta}$ induced an increase in Bax, and a decrease in Bcl-2 compared to the controls. However, a pre-treatment with chlorogenic acid rescued the PC12 cells from A${\beta}$ by attenuating the elevated intracellular calcium levels and reducing the levels of the apoptosis related proteins, including caspase-3, Bcl-2 and Bax. These results suggest that the protective effects of chlorogenic acid are, at least in parts, by attenuating the intracellular calcium influx and reducing apoptosis induced by A${\beta}$.

• 대한생식의학회:학술대회논문집
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• 2002.11a
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• pp.94-95
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• 2002

• Fisheries and Aquatic Sciences
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• v.1 no.2
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• pp.293-295
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• 1998