• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.537-546
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• 1997

It has been postulated that the intracellular taurine is co-transported with $Na^+$down a concentration gradient and prevents the intracellular accumulation of sodium. It is therefore, expected that an elevated level of intracellular taurine prevents the sodium-promoted calcium influx to protect the cellular damages associated with sodium and calcium overload. In the present study, we evaluated the effects of intra- and extracellular taurine on the myocardial $Na^+$and$Ca^{++}$ contents and the cardiac functions in isolated rat hearts which were loaded with sodium by monensin, a $Na^+-ionophore$. Monensin caused a dose-dependent increase in intracellular $Na^+$ accompanied with a subsequent increase in intracellular $Ca^{++}$ and a mechanical dysfunction. In this monensin-treated heart, myocardial taurine content was decreased with a concomittent increase in the release of taurine. The monensin-induced increases in intracellular $Na^+$, $Ca^{++}$ and depression of cardiac function were prevented in the hearts of which taurine content had been increased by high-taurine diet. Conversely, in the hearts of which taurine concentration gradient had been decreased by addition of taurine in the perfusate, the monensin-induced increases in $Na^+$, $Ca^{++}$ and functional depression were accelerated. These results suggest that taurine, depending on the intra-extracellular concentration gradient, can affect intracellular sodium and calcium concentrations, and that an increased intracellular taurine may play a role in protection of myocardial dysfunction associated with the sodium and calcium overload.

• Journal of the East Asian Society of Dietary Life
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• v.9 no.3
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• pp.378-385
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• 1999

A reduced NaCl intake for the general population of the world has been recommended to reduce the overall blood pressure level and hence to reduce the overall incidence of cardiovascular disease. A high NaCl diet convincingly contributes to elevated arterial pressure in humans and animal models of hypertension. Among individuals there is considerable variability of blood pressure responsiveness to NaCl intake. In normotensive as well as hypertensive subjects, blood pressure can be judged to be salt sensitivity (SS) when observed to vary directly and substantially with the net intake of NaCl. The prevalence of SS in normotensive adults in the U.S. ranges from 15% to 42% and in hypertensive adults from 28% to 74%. SS is a risk factor for hypertension and may be an important marker in the identification of children for hypertension prevention programs. High NaCl intakes produce expansion of the extracellular fluid volume and thus increase blood pressure. Nonchloride salts of sodium does not expand the extracellular fluid volume and does not alter blood pressure. Blood pressure response to NaCl may be modified by other components of the diet. Low dietary intakes of potassium or calcium augment NaCl-induced increases of blood pressure. Conversely, high dietary intakes of potassium or calcium attenuate NaCl-induced hypertension. A greater intakes of potassium or calcium may prevent or delay the occurrence of hypertension. SS occurs when dietary potassium is even marginally deficient but is dose-dependently suppressed when dietary potassium is increased within its normal range. Orally administered KHCO$_3$, abundant in fruits and vegetates, but not KCl has a calcium-retaining effect which may contributed to its reversal of pressor effect of dietary NaCl. Since nutrients other than NaCl also affect blood pressure levels, a reduced NaCl intake should be only one component of a nutritional strategy to lower blood pressure.

• Annals of dermatology
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• v.30 no.6
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• pp.751-754
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• 2018

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.5
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• pp.345-356
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• 2019

Docosahexaenoic acid (DHA), an omega-3-fatty acid, modulates multiple cellular functions. In this study, we addressed the effects of DHA on human umbilical vein endothelial cell calcium transient and endothelial nitric oxide synthase (eNOS) phosphorylation under control and adenosine triphosphate (ATP, $100{\mu}M$) stimulated conditions. Cells were treated for 48 h with DHA concentrations from 3 to $50{\mu}M$. Calcium transient was measured using the fluorescent dye Fura-2-AM and eNOS phosphorylation was addressed by western blot. DHA dose-dependently reduced the ATP stimulated $Ca^{2+}$-transient. This effect was preserved in the presence of BAPTA (10 and $20{\mu}M$) which chelated the intracellular calcium, but eliminated after withdrawal of extracellular calcium, application of 2-aminoethoxy-diphenylborane ($75{\mu}M$) to inhibit store-operated calcium channel or thapsigargin ($2{\mu}M$) to delete calcium store. In addition, DHA ($12{\mu}M$) increased ser1177/thr495 phosphorylation of eNOS under baseline conditions but had no significant effect on this ratio under conditions of ATP stimulation. In conclusion, DHA dose-dependently inhibited the ATP-induced calcium transient, probably via store-operated calcium channels. Furthermore, DHA changed eNOS phosphorylation suggesting activation of the enzyme. Hence, DHA may shift the regulation of eNOS away from a $Ca^{2+}$ activated mode to a preferentially controlled phosphorylation mode.

• Applied Biological Chemistry
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• v.31 no.2
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• pp.187-192
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• 1988

Extracellular protein was produced from bacterium, which was classified as a strain belong to the genus Bacillus. This bacterium produced 1.4mg/ml of extracellular protein when grown on chemically defined medium containing 3.0% of glucose, 1.3% of urea and 2.5% of calcium carbonate at $30^{\circ}C$ for 48 hours. The addition of $250{\mu}g/ml$ of cephalexin was effective for it and was produced 2.0mg/ml of extracellular protein for 96 hours.

• Journal of Microbiology
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• v.34 no.3
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• pp.253-269
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• 1996

Infection of fish cells with IHNV resulted in gradual increase in cytosolic free Ca$\^$2+/ concentration ([Ca$\^$2+/)] in CHSE, gradual decrease in [Ca$\^$2+/] in FHM, and no significant change in RTG cells. The degree of [Ca$\^$2+/] increase or decrease was dependent on the amount of infectious virus, and these [Ca$\^$2+/] variations were maximal at 16 hours after virus infection (p. i.) in both cell lines. When the fish cells were infected with inactivated IHNV, evident variation in [Ca$\^$2+/] was not observed. Thus, infectivity of IHNV appears to correlate with changes in [Ca$\^$2+/] in virus-infected cells. These IHNV-induced [Ca$\^$2+/] changes were partially blocked by cycloheximide, but not affected by cordycepin. It seems to be that virus-induced Ca$\^$2+/ variations were more related with protein synthesis than RNA synthesis. Various Ca$\^$2+/ related drugs were used in search for the mechanisms of the [Ca$\^$2+/], changes following IHNV infection of CHSE cells. Decreasing extracellular Ca$\^$2+/ concentration or blocking Ca$\^$2+/ influx from extracellular media inhibited the IHNV-induced increase in [Ca$\^$2+/], in CHSE cells. Similar results were obtained with intracellular Ca$\^$2+/ sources are important in IHNV-induced [Ca$\^$2+/] increase in CHSE cells.

• Clinical and Experimental Reproductive Medicine
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• v.14 no.2
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• pp.93-100
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• 1987

To determine the effect of calcium on the preimplantational development of mouse two-cell embryo, the various concentrations of calcium were added into the culture media and the rate of blastocyst formation was observed. Also, to examine the effect of trifluoperazine, an inhibitor of calmodulin which is involved in the several intracellular calcium functions, embryos were cultured for 48 hours at the various concentrations of this inhibitor. An additional 24 hour culture was done to examine the effect of this drug on the transformation from morula to blastocyst. The results are as following ; 1. About 1.71mM of extracellular calcium is adequate for blastocyst formation and the higher concentrations of calcium (3.43mM and 8.55mM) do not affect on the blastocyst formation and the degenerating rate. 2. Trifluoperazine $100{\mu}M$ presents the inhibitory effect on the blastocyst formation while $1{\mu}M$ and $10{\mu}M$ do not so. 3. After an additional 24 hour culture, there is transformation of morula to blastocyst and the degenerating rate of embryo is increased all together.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.371-379
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• 2016

Store-operated calcium entry (SOCE), a major mode of extracellular calcium entry, plays roles in a variety of cell activities. Accumulating evidence indicates that the intracellular calcium ion concentration and calcium signaling are critical for the responses induced by oxidative stress. The present study was designed to investigate the potential effect of SOCE inhibition on $H_2O_2$-induced apoptosis in endothelial progenitor cells (EPCs), which are the predominant cells involved in endothelial repair. The results showed that $H_2O_2$-induced EPC apoptosis was reversed by SOCE inhibition induced either using the SOCE antagonist ML-9 or via silencing of stromal interaction molecule 1 (STIM1), a component of SOCE. Furthermore, SOCE inhibition repressed the increases in intracellular reactive oxygen species (ROS) levels and endoplasmic reticulum (ER) stress and ameliorated the mitochondrial dysfunction caused by $H_2O_2$. Our findings provide evidence that SOCE inhibition exerts a protective effect on EPCs in response to oxidative stress induced by $H_2O_2$ and may serve as a potential therapeutic strategy against vascular endothelial injury.

• Biomedical Science Letters
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• v.13 no.4
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• pp.333-339
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• 2007

Recently, much attention has been paid to human retinoblastoma since it provide a good model system for studying mechanisms underlying cell growth, differentiation, proliferation, and apoptosis, and for developing cancer therapy. However, until now it is unclear whether purinergic receptors are involved in the calcium mobilization in the retinoblastoma cells. In this regard, we measured possible purinergic signaling in WERI-Rb-1 cells using $Ca^{2+}$ imaging technique and RT-PCR method. ATP-induced $[Ca^{2+}]_i$ transients was maintained to about $90.7{\pm}1.0%$ of the control (n=48) even in the absence of extracellular calcium. The ATP-induced intracellular calcium response was only attained to $10.4{\pm}1.8%$ (n=55) of peak amplitude of the control after preincubation of 1 ${\mu}MU-73122$, a PLC inhibitor, but it was not affected by 1 ${\mu}MU-73343$, a inactive form of U-73122. And also ATP-induced $[Ca^{2+}]_i$ rise was almost attenuated by 20 ${\mu}M$ 2-APB, a putative $IP_3$ receptor inhibitor. Two subtypes of $IP_3$ receptor $(IP_{3-1}R,\;IP_{3-2}R)$ were identified by a RT-PCR method. These findings suggest that purinergic stimuli can cause calcium mobilization via $PLC-IP_3$ pathway after the activation of P2Y receptors in the retinoblastoma cells, which may play important roles in cell proliferation, differentiation, growth, and cell death.

• International Journal of Oral Biology
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• v.33 no.1
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• pp.33-43
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• 2008

In the process of bone remodeling, mineral phase of bone is dissolved by osteoclasts, resulting in elevation of calcium concentration in micro-environment. This study was performed to explore the effect of high extracellular calcium ($Ca{^{2+}}_e$) on mineralized nodule formation and on the expression of progressive ankylosis (Ank), plasma cell membrane glycoprotein-1 (PC-1) and osteopontin by primary cultured mouse calvarial cells. Osteoblastic differentiation and mineralized nodule formation was induced by culture of mouse calvarial cells in osteoblast differentiation medium containing ascorbic acid and ${\beta}$-glycerophosphate. Although Ank, PC-1 and osteopontin are well known inhibitors of mineralization, expression of these genes were induced at the later stage of osteoblast differentiation during when expression of osteocalcin, a late marker gene of osteoblast differentiation, was induced and mineralization was actively progressing. High $Ca{^{2+}}_e$(10 mM) treatment highly enhanced mRNA expression of Ank, PC-1 and osteopontin in the late stage of osteoblast differentiation but not in the early stage. Inhibition of p44/42 MAPK activation but not that of protein kinase C suppressed high $Ca{^{2+}}_{e^-}$induced expression of Ank, PC-1 and osteopontin. When high $Ca{^{2+}}_e$(5 mM or 10 mM) was present in culture medium during when mineral deposition was actively progressing, matrix calcifiation was significantly increased by high $Ca{^{2+}}_e$. This stimulatory effect was abolished by pyrophosphate (5 mM) or levamisole (0.1-0.5 mM), an alkaline phosphatase inhibitor. In addition, probenecid (2mM), an inhibitor of Ank, suppressed matrix calcification in both control and high $Ca{^{2+}}_{e^-}$treated group, suggesting the possible role of Ank in matrix calcification by osteoblasts. Taken together, these results showed that high $Ca{^{2+}}_e$ stimulates expression of Ank, PC-1 and osteopontin as well as matrix calcification in late differentiation stage of osteoblasts and that p44/42 MAPK activation is involved in high $Ca{^{2+}}_{e^-}$induced expression of Ank, PC-1 and osteopontin.