• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1999년도 학술발표회 진행표 및 논문초록
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• pp.68-68
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• 1999

Extracellular A TP is known to function as a neurotransmitter and as a modulator in the variety of cell types. In PC12 cells, extracellular A TP elevates [Ca$\^$2＋/]j through receptor-operated Ca$\^$2＋/ channels and through the activation of phospholipase C, thereby facilitating the secretion of neurotransmitters.(omitted)

• Journal of Microbiology
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• 제34권3호
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• pp.263-263
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• 1996

Infection of fish cells with IHNV resulted in gradual increase in cytosolic free $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in CHSE, gradual decrease in $[Ca^{2+}]_i$ in FHM, and no significant change in RTG cells. The degree of $[Ca^{2+}]_i$ increase or decrease was dependent on the amount of infectious virus, and these $[Ca^{2+}]_i$ 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 $[Ca^{2+}]_i$ was not observed. Thus, infectivity of IHNV appears to correlate with changes in $[Ca^{2+}]_i$ in virus-infected cells. These IHNV-induced $[Ca^{2+}]_i$ 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 $[Ca^{2+}]_i$, 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 $[Ca^{2+}]_i$, in CHSE cells. Similar results were obtained with intracellular $Ca^{2+}$ blockers. Thus it is suggested that both the extracellular and the intracellular $Ca^{2+}$ sources are important in IHNV-induced $[Ca^{2+}]_i$ increase in CHSE cells.

• 생명과학회지
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• 제25권2호
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• pp.231-236
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• 2015

Angiotensin II (AngII)는 혈관평활근세포의 수축을 통해 혈관을 수축시키는 강력한 작용을 나타낼 뿐만 아니라 혈관세포의 성장 등에 중요한 역할을 한다. 본 연구에서는 AngII에 의해 형성되는 활성산소가 phosphatidylinositol 3-kinase (PI3K)에 유리되는 칼슘에 의해 조절된다는 것을 검증하였다. 쥐의 대동맥으로부터 분리된 혈관평활근세포에서 AngII에 의해 활성산소가 농도 의존적, 그리고 시간 의존적으로 형성됨을 관찰하였다. AngII에 의해 형성되는 활성산소는 PI3K의 억제제에 의해 봉쇄되었으나 EKR의 억제제에 의해서는 봉쇄되지 않음을 알 수 있었다. AngII에 의해 유리되는 칼슘은 L-type 칼슘이온통로 봉쇄제인 Nifedipine 또는 배양액에 칼슘이 제거된 환경에서 억제됨을 확인할 수 있었다. 마지막으로 AngII에 의해 형성되는 활성산소는 배양액에 칼슘이 없는 조건이나 L-type 칼슘이온통로 억제제를 전처리 하였을 경우 억제되는 것을 확인하였다. 이러한 결과들을 바탕으로 쥐의 대동맥으로부터 분리된 혈관평활근세포에서 AngII에 의한 활성산소의 형성은 PI3K/L-type 칼슘이온통로를 통한 기전을 통해 조절됨을 제안한다.

• 약학회지
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• 제41권2호
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• pp.212-219
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• 1997

Multiple forms of extracellular phospholipase $A_2$ have been detected in human amniotic fluid (HAF). When HAF was subjected to heparin-Sepharose column chromatography, phospholipase $A_2$ activity was detected in both heparin-non binding and binding fraction. The activity of heparin-non binding fraction was further purified by sequential uses of column chromatographies on butyl-Toy-opearl 650M and DEAE-Sephacel. DEAE-Sephacel fraction contained three different phospholipase $A_2$ activities (Peak I, II, III). The molecular weight of DEAE-Sephacel fraction phospholipase $A_2$ determined by SDS-PAGE were about 52KDa (Peak I). Peak II, III required micromolar $Ca^{2+}$ ion for its maximum activity, but Peak I enzyme showed calcium independent phospholipase $A_2$ activity and showed broad range of pH (6.0~10.0) optimum. All these enzymes were not recognized by a monoclonal antibody raised against phospholipase $A_2$ from human synovial fluid. These results suggest that HAF might contain multiple forms of extracellular phospholipase $A_2$, which may neither belong to the 14KDa group II phospholipase $A_2$ family nor cytosolic phospholipase $A_2$.

• Journal of Plant Biology
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• 제39권2호
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• pp.113-121
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• 1996

The role of Ca2+ on benzyladenine (BA)-induced senescence retardation in mature wheat (Triticum aestivum L.) primary leaves was investigated. When an extracellular calcium chelator, ethylene glycol-bis-($\beta$-aminoethylether)-N, N'-tetraacetic acid (EGTA) together with BA, was applied to senescing leaves for 4 days of dark incubation, the content of chlorophyll and soluble protein decreased rapidly. And, the content of malondialdehyde (MDA), known to be a degradation product of membrane lipids, increased compared with the BA alone control. The BA-EGTA combination also caused the stimulation of protease and RNase activity and a rapid loss of catalase activity owing to the decling of BA effects. In the case of treatment with only intracellular calcium antagonist 3, 4, 5-trimethoxybenzoic acid 8-(diethylamino) octyl ester (TMB-8) without the BA addition, the chlorophyll content at day 4 after dark incubation decreased in paralled with the increasing concentration of the antagonist. In addition, the chlorophyll content at 10-5 M calcium ionophore A23187 treatment in the absence of BA was similar to that of the BA alone treatment. These results suggest that calcium may mediate the retardation effect of BA on leaf senescence by acting as a second messenger and that the calcium input from cell organelles, as well as the calcium inflow from intercellular spaces and cell walls, may be involved in modulating cytosolic calcium levels related to BA action.

• Clinical and Experimental Reproductive Medicine
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• 제23권3호
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• pp.357-366
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• 1996

The present experiments aimed to investigate the metabolism of calcium during oocyte maturation in rat. The concentration of free calcium and calmodulin in oocytes was measured respectively by using of fluo-3/AM and FITC with microscope fluorescence spectrometer. The ultrastructural localization of calcium precipitates in oocytes was observed with the transmission electron microscope. Cumulus-free immature oocytes(GV-oocyte) were cultured in vitro through 15 hours. The free calcium concentration in GV oocyte was $55.9{\pm}3.5nM$. In calcium-containing medium, the free calcium concentration was increased in germinal vesicle breakdown(GVBD) oocyte($64.2{\pm}7.3nM$). In normal medium after calcium chelator treatment ($10{\mu}M$ BAPTA/AM), the free calcium contents were slightly lower than those in control group. In calcium-free medium, the free calcium content was drastically increased in GVBD($72.7{\pm}3.4nM$) and metaphase I - anaphase I ($88.0{\pm}3.4nM$) oocyte. In maturation rate of oocytes, GVBD rate was high in control group($82.9{\pm}6.55%$) and calcium chelator treatment group($91.2{\pm}4.4%$), but in calcium-free medium group, it was low and then the oocyte was degenerated without polar body formation. Relative content of calmodulin in oocyte was significantly(P<0.001) increased in metaphase I - anaphase I than in GV and GVBD oocyte. The calcium precipitates were observed in mitochondria and cytoplasm of GV oocyte but that were not observed in mitochondria of GVBD and metaphase I - anaphase I oocyte. And then the calcium precipitates reappeared in mitochondria of metaphase II oocyte. The above results indicate that changes in free calcium and calmodulin concentration of oocyte occur according to the maturational stages and the extracellular calcium is required during oocyte maturation. Also change of calcium localization in oocyte occurs according to the maturational stages.

• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3561-3568
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• 2012

The calcium sensing receptor (CaSR) is a member of the largest family of cell surface receptors, the G protein-coupled receptors involved in calcium homeostasis. The role of the CaSR in neoplasia appears to be homeostatic; loss of normal CaSR-induced response to extracellular calcium is observed in cancers of the colon and ovary, while increased release of PTHrP is observed in cancers of the breast, prostate and Leydig cells. Currently CaSR can be considered as a molecule that can either promote or prevent tumor growth depending on the type of cancer. Therefore, recognition of the multifaceted role of CaSR in gliomas and other malignant tumors in general is fundamental to elucidating the mechanisms of tumor progression and the development of novel therapeutic agents. Emphasis should be placed on development of drug-targeting methods to modulate CaSR activity in cancer cells.

• International Journal of Oral Biology
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• 제35권3호
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• pp.129-135
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• 2010

Recent studies have implicated reactive oxygen species (ROS) as determinants of the pathological pain caused by the activation of peripheral neurons. It has not been elucidated, however, how ROS activate the primary sensory neurons in the pain pathway. In this study, calcium imaging was performed to investigate the effects of NaOCl, a ROS donor, on the intracellular calcium concentration ($[Ca^{2+}]i$) in acutely dissociated dorsal root ganglion (DRG) neurons. DRG was sequentially treated with 0.2 mg/ml of both protease and thermolysin, and single neurons were then obtained by mechanical dissociation. The administration of NaOCl then caused a reversible increase in the $[Ca^{2+}]i$, which was inhibited by pretreatment with phenyl-N-tertbuthylnitrone (PBN) and isoascorbate, both ROS scavengers. The NaOCl-induced $[Ca^{2+}]i$ increase was suppressed both in a calcium free solution and after depletion of the intracellular $Ca^{2+}$ pool by thapsigargin. Additionally, this increase was predominantly blocked by pretreatment with the transient receptor potential (TRP) antagonists, ruthenium red ($50\;{\mu}M$) and capsazepine ($10\;{\mu}M$). Collectively, these results suggest that an increase in the intracellular calcium concentration is produced from both extracellular fluid and the intracellular calcium store, and that TRP might be involved in the sensation of pain induced by ROS.

• Animal cells and systems
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• 제7권1호
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• pp.75-79
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• 2003

Highly purified high performance thin layer chromatography (HPTLC) fractions containing a putative calcium influx factor (CIF) were prepared from the Jurkat cells and Xenopus oocytes in which $Ca^{2+}$ stores were depleted by thapsigargin treatment and from the yeast in which intracellular $Ca^{2+}$ stores were also depleted by genetic means. Microinjection of the fractions has been shown to elicit $Ca^{2+}$ dependent currents in Xenopus oocytes. The nature of the membrane currents evoked by the putative CIF appeared to be carried by chloride ions since the current was blocked by the selective chloride channel blocker 1 mM niflumic acid and its reversal potential was about -24 mV. Injection of the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N, N, N',N'-tetraacetic acid (BAPTA) eradicated the current activities, suggesting the current responses are entirely $Ca^2$-dependent. Moreover, the currents were sensitive to the removal of extracellular calcium, indicating the dependence on calcium entry through the plasma membrane calcium entry channels. CIF activities were insensitive to protease, heat, and acid treatments and to Dische-reaction whereas the activities were sensitive to nucleotide pyrophosphatase and hydrazynolysis. The fraction might have a sugar because it was sensitive to Molisch test and Seliwaniff's resorcinol reaction. From the above results, CIF as a small and stable molecule seems to have pyrimidine, pyrophosphate, and a sugar moiety.oiety.

• International Journal of Oral Biology
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• 제49권2호
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• pp.34-41
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• 2024

Extracellular traps (ETs), primarily composed of DNA and antibacterial peptides, are mainly secreted by neutrophils to inhibit pathogen spread and eliminate microorganisms. Recent reports suggest that microglia can also secrete ETs, and these microglial ETs are associated with various neurological conditions, including nerve injury, tumor microenvironment, and ischemic stroke. However, the components and functions of microglial ETs remain underexplored. Secretagogin (Scgn), a calcium-sensor protein, plays a crucial role in the release of peptide hormones, such as insulin, in endocrine cells; however, its function in immune cells, including microglia, is not well understood. Our study demonstrated that Scgn deficiency can lead to the formation of abnormal ETs. We hypothesized that this may involve the c-Jun N-terminal kinase-myeloperoxidase pathway and autophagy.