• 대한약리학회지
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• 제22권2호
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• pp.151-156
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• 1986

최근 심근세포 또는 신경세포에서 발표된 여러 종류의 calcium channel중 calcium antagonist로 차단되는 channel 또는 차단되지 않는 channel 등이 있는지 알아보기 위해 실험을 시행하였다. 돼지 소장 평활근으로부터 고농도의 KCl(150mM)로 부하된 세포 포막낭을 만들어 고농도의$K^+$ 또는 전기자극으로 $^{45}Ca$의 이동을 유발시켜 다음과 같은 성적을 얻었다. 저농도의 $K^+$용액에서의 $^{45}Ca$이동보다 고농도의 $K^+$-용액에서의 $^{45}Ca$이동이 유의하게 증가되었으며(p<0. 05) 이때 유입되는 $^{45}Ca$의 양은 시간에 따라 서서히 감소되었다. 전기자극(3V, 15Hz, 25msec)을 하였을때 유입되는 $^{45}Ca$의 양은 전기자극을 하지 않은 대조군에 비하여 현저하게 증가되었고, 자극시간에 따른 $^{45}Ca$의 유입량은 2분 동안 계속 증가되었다. Diltiazem 또는 nifedipine을 처치하였을때, 고농도의 $K^+$-용액에 의한 $^{45}Ca$의 유입은 억제되지 않았으나 전기자극에 의해 유도되는 $^{45}Ca$의 유입은 유의하게 억제되었다(p<0.005). 상기의 실험성적으로 돼지 소장 평활근으로부터 분리한 세포막에서의 calcium이동 중 전기자극에 의해 이루어지는 것은 calcium antagonist로 차단되는 calcium channel을 통하여 이루어지는 것으로 사료된다.

• 대한약리학회지
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• 제31권3호
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• pp.355-363
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• 1995

Calcium수송에 대한 기전을 추구하기위하여, carbachol을 사용하여 ml muscarinic receptor-transfected RBL-2H3 cell-line에서 다음과 같은 실험결과를 얻었기에 이에 보고한다. 1) Carbachol의 투여로 이들 cell-line에서 $Ca^{2+}$ influx가 농도에 따라 증가하였고, hexosaminidase 분비양도 의의있게 증가하였다. 2) Atropine 투여로 Carbachol의 상승작용이 의의있게 억제되었다. 3) 수종의 금속양이온을 투여하여 carbachol의 $Ca^{2+}$수송에 대한 영향을 관찰한 바, 이들 금속이온들은 $Ca^{2+}$의 influx를 의의있게 억제하였다. 4) PMA(20 nM) 투여로 carbachol의 hexosaminidase의 분비는 억제되지 못했지만 $Ca^{2+}$ influx는 억제되었다. 5) PTx $(0.2\;{\mu}g/ml)$ 투여로 carbachol의 hexosaminidase 분비가 의의있게 억제되었다. 위의 결과로 미루어 보아, 이 세포의 muscarinic receptor가 calcium channel을 통한 calcium수송에 매우 중요한 영향을 나타내는데, 이들 calcium ion channel은 적어도 두 종류가 존재하며, 하나는G-protein-dependent calcium channel에 의하며, 다른 하나는 G-protein-independent calcium channel에 대한 작용에 의한 것으로 생각된다. 또한 이 calcium channel들은 2가 또는 3가의 다른 금속 ion들에 의하여 calcium수송이 억제된다.

• Journal of Plant Biology
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• 제36권1호
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• pp.59-66
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• 1993

In maize coleoptile segments where auxin transport capacity decreases with time following excision, susceptability of the tissue to transport inhibitors such as N-1-naphthylphthalamic acid (NPA), 3,4,5-triiodobenzoic acid (TIBA) or high concentrations of IAA was found to be rather increased. A time-dependent increase in the sensitivity to NPA can be postulated since the dose-response curve for NPA was shifted in the‘aged’tissue to the left (i.e. lower concentration). Preincubation of the tissue at a low temperature abolished the time-dependent sensitivity change, suggesting that cellular metabolism could be involved. The NPA-sensitive state was also brought about by calcium depletion of the tissue, which can be partially reversed by addition of calcium. Presence of exogenous IAA in the preincubation medium kept the auxin transport system from decay, implicating auxin as an endogenous controlling factor. Results of our experiments indicate a reversible, time-dependent changes of auxin transport system in which transport capacity and sensitivity to NPA are tightly coupled. Changes in the sensitivity to NPA were also seen in auxin action as well.

• Journal of Pharmaceutical Investigation
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• 제38권5호
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• pp.295-302
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• 2008

In the present study, we examined the changes of uptake and efflux of taurine under various conditions inducing oxidative stress using rat conditionally immortalized syncytiotrophoblast cell line, TR-TBT cell, as blood-placental barrier in vitro model. In addition, we identified the characteristics of taurine transport in TR-TBT cells including general features, besides effect of calcium ion on taurine transport. Taurine uptake showed time, $Na^+$ and $Cl^-$ dependency, and was decreased by PKC activator in TR-TBT cells. Also, calcium free condition decreased taurine uptake and evoked taurine efflux in the cells. Oxidative stress induced the change of taurine transport in TR-TBT cells, but the changes were different depending on the types of stimulation inducing oxidative stress. The taurine uptake was increased by TNF-$\alpha$, LPS and DEM stimulation but decreased by $H_2O_2$ and NO stimulation. Also, the taurine efflux was regulated by TNF-$\alpha$ stimulation. In conclusion, the taurine transport through the blood-placental barrier was regulated in oxidative stress conditions, and these results demonstrated that oxidative stress affected the taurine supplies to fetus and taurine level of fetus.

• The Korean Journal of Physiology
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• 제10권1호
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• pp.1-5
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• 1976

The trypanocidal drug suramin, an impermeant polyanion, has been shown to be a powerful inhibitor of the calcium uptake and calcium-stimulated ATPase activity of sarcoplasmic reticulum (Fortes et al., 1974). In view of this finding, an attempt was made to investigate the effect of suramin on $Ca^{++}$ transport in resealed red cells and on $Ca^{++}$-activated ATPase in red blood cell membrane fragments (RBCMF). The results obtained are summarized as follows. 1. $Ca^{++}$ outflux from the resealed RBC was inhibited by suramin and the inhibitory action of suramin is proportional to the concentration of drug added inside the RBC preparation. When suramin is added both inside and outside the RBC preparation simultaneously, the magnitude of the inhibitory effect was more pronounced, suggesting that suramin inhibits both active $Ca^{++}-^{45}Ca$ exchange diffusion across the RBC membrane. 2. Suramin inhibits the $Ca^{++}$-activated ATPase of the RBCMF and the effect of inhibition by the drug was also concentration dependent. From the above results, it may be concluded that suramin inhibits $Ca^{++}$ transport across RBC membrane by inhibiting $Ca^{++}$-activated ATPase activity which has been known to be linked with active $Ca^{++}$ transport.

• Journal of Plant Biology
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• 제32권4호
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• pp.343-350
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• 1989

Calcium promoted ethylene production from mungbean hypocotyl segments incubated in the presence of either auxin or cytokinin (kinetin). Time course studies indicated that the calcium effect on ethylene production had a longer latent period (about 6 h) in combination with kinetin than with auxin. Studies on the effects of agents that are known to interfere with either action or transport (uptake) of calcium on ethylene biosynthesis indicated different patterns between auxin- and kinetin-treated tissues. Auxin-induced ethylene production was inhibited by the calmodulin inhibitor, trifluoperazine (TFP), and this inhibition was overcome by high concentrations of calcium applied, but TFP had no significant effect on kinetin-induced ethylene production regardless of calcium in the medium. The calcium channel blocker, verapamil, inhibited auxin-induced, but had little effect on kinetin-induced, ethylene producton. In vivo activity of "ethylene forming enzyme (EFE)" was found to be substantially promoted by calcium treatment. The enzyme activity was further increased by kinetin when segments were simultaneously treated with calcium, but auxin did not have such an effect.an effect.

• Molecules and Cells
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• 제45권11호
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• pp.855-867
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• 2022

For proper function of proteins, their subcellular localization needs to be monitored and regulated in response to the changes in cellular demands. In this regard, dysregulation in the nucleocytoplasmic transport (NCT) of proteins is closely associated with the pathogenesis of various neurodegenerative diseases. However, it remains unclear whether there exists an intrinsic regulatory pathway(s) that controls NCT of proteins either in a commonly shared manner or in a target-selectively different manner. To dissect between these possibilities, in the current study, we investigated the molecular mechanism regulating NCT of truncated ataxin-3 (ATXN3) proteins of which genetic mutation leads to a type of polyglutamine (polyQ) diseases, in comparison with that of TDP-43. In Drosophila dendritic arborization (da) neurons, we observed dynamic changes in the subcellular localization of truncated ATXN3 proteins between the nucleus and the cytosol during development. Moreover, ectopic neuronal toxicity was induced by truncated ATXN3 proteins upon their nuclear accumulation. Consistent with a previous study showing intracellular calcium-dependent NCT of TDP-43, NCT of ATXN3 was also regulated by intracellular calcium level and involves Importin α3 (Imp α3). Interestingly, NCT of ATXN3, but not TDP-43, was primarily mediated by CBP. We further showed that acetyltransferase activity of CBP is important for NCT of ATXN3, which may acetylate Imp α3 to regulate NCT of ATXN3. These findings demonstrate that CBP-dependent acetylation of Imp α3 is crucial for intracellular calcium-dependent NCT of ATXN3 proteins, different from that of TDP-43, in Drosophila neurons.

• Journal of Plant Biotechnology
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• 제39권1호
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• pp.23-32
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• 2012

Calcium is an essential nutrient for living organisms, with key structural and signaling roles. Its deficiency in plants can result in poor biotic and abiotic stress tolerance as well as reduced crop quality and yield. Calcium deficiency in humans causes various diseases such as osteoporosis and rickets. Biofortification of calcium in various food crops has been suggested as an economic and environmentally advantageous method to enhance human intake of calcium. Recent efforts to increase the levels of calcium in food crops have used calcium/proton antiporters ($CAXs$) and modified one to increase calcium transport into vacuoles through genetic engineering. It has been reported that overall calcium content of transgenic plants has been increased in their edible portions with some adverse effects. In conclusion, biofortification of calcium will add more value in crops as well as will be beneficial for animal and human. Therefore, more fundamental studies on the mechanisms of calcium ion storage and transporting are essential for more effective calcium biofortification.

• 대한약리학회:학술대회논문집
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• 대한약리학회 2006년도 The 6th Congress of the Federation of Asian and Oceanian Physiological Societies
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• pp.96.2-96.2
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• 2006

• Biomolecules & Therapeutics
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• 제16권3호
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• pp.219-225
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• 2008

Taurine is the most abundant amino acid in many tissues and is found to be enhancing the bone tissue formation or inhibits the bone loss. Although it is reported that taurine reduces the alveolar bone loss through inhibiting the bone resorption, its functions of taurine and expression of taurine transporter (TauT) in bone have not been identified yet. The purpose of this study is to clarify the uptake mechanism of taurine in osteoblast using mouse osteoblast cell lines. In this study, mouse stromal ST2 cells and mouse osteoblast-like MC3T3-E1 cells as osteoblast cell lines were used. The activity of taurine uptake was assessed by measuring the uptake of [$^3H$]taurine in the presence or absence of inhibitors. TauT mRNA was detected in ST2 and MC3T3-E1 cells. [$^3H$]Taurine uptake by these cells was dependent on the presence of extracellular calcium ion. The [$^3H$]taurine uptake in ST2 cells treated with 4 mM calcium was increased by 1.7-fold of the control which was a significant change. In contrast, in $Ca^{++}$-free condition and L-type calcium channel blockers (CCBs), taurine transport to osteocyte was significantly inhibited. In oxidative stress conditions, [$^3H$]taurine uptake was decreased by TNF-$\alpha$ and $H_2O_2$. Under the hyperosmotic conditions, taurine uptake was increased, but inhibited by CCBs in hyperosmotic condition. These results suggest that, in mouse osteoblast cell lines, taurine uptake by TauT was increased by the presence of extracellular calcium, whereas decreased by CCBs and oxidative stresses, such as TNF-$\alpha$ and $H_2O_2$.