• 한국작물학회:학술대회논문집
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• 한국작물학회 2006년도 한국약용작물학회 공동춘계학술발표회
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• pp.294-295
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• 2006

• Toxicological Research
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• 제14권4호
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• pp.507-513
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• 1998

The purpose of this study was to clarify the effect of silica on cytosolic free calcium mobilization and cell injury in primary cultured rat hepatocytes. Cytosolic free calcium concentration ([Ca$^{2+}$]) was measured employing calcium sensitive fluorescent dye, Fura-2 / AM, and cell injury was evaluated by determination of cellular ATP contents. Silica increased [Ca$^{2+}$], in a concentration-dependent manner in hepatocytes (10$^{-5}$ ~10$^{-2}$ M). Silica caused a biphasic increase in [Ca$^{2+}$], which was composed of an initial rapid rise and following sustained phase. $Ca^{2+}$ removal from the medium resulted in abolishment of initial and sustained phase of silica (10$^{-2}$ M)-induced [Ca$^{2+}$], in hepatocytes. The pretreatment with nifedipine (1 $\mu$M) attenuated silica-induced [Ca$^{2+}$], increases. Silica decreased cellular ATP contents in a dose-dependent manner. This silica-induced cell injury was attenuated by the pretreatment with EGTA (100 $\mu$M) and nifedipine (1 $\mu$M). This study suggests that the elevation of [Ca$^{2+}$], caused by silica may be due mainly to influx through a plasma membrane $Ca^{2+}$ channel and hepatotoxicity by silica relate with alteration of calcium homeostasis.ium homeostasis.

• Molecules and Cells
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• 제43권1호
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• pp.66-75
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• 2020

Saturated fatty acids contribute to β-cell dysfunction in the onset of type 2 diabetes mellitus. Cellular responses to lipotoxicity include oxidative stress, endoplasmic reticulum (ER) stress, and blockage of autophagy. Palmitate induces ER Ca²⁺ depletion followed by notable store-operated Ca²⁺ entry. Subsequent elevation of cytosolic Ca²⁺ can activate undesirable signaling pathways culminating in cell death. Mitochondrial Ca²⁺ uniporter (MCU) is the major route for Ca²⁺ uptake into the matrix and couples metabolism with insulin secretion. However, it has been unclear whether mitochondrial Ca²⁺ uptake plays a protective role or contributes to lipotoxicity. Here, we observed palmitate upregulated MCU protein expression in a mouse clonal β-cell, MIN6, under normal glucose, but not high glucose medium. Palmitate elevated baseline cytosolic Ca²⁺ concentration ([Ca²⁺]_i) and reduced depolarization-triggered Ca²⁺ influx likely due to the inactivation of voltage-gated Ca²⁺ channels (VGCCs). Targeted reduction of MCU expression using RNA interference abolished mitochondrial superoxide production but exacerbated palmitate-induced [Ca²⁺]_i overload. Consequently, MCU knockdown aggravated blockage of autophagic degradation. In contrast, co-treatment with verapamil, a VGCC inhibitor, prevented palmitate-induced basal [Ca²⁺]_i elevation and defective [Ca²⁺]_i transients. Extracellular Ca²⁺ chelation as well as VGCC inhibitors effectively rescued autophagy defects and cytotoxicity. These observations suggest enhanced mitochondrial Ca²⁺ uptake via MCU upregulation is a mechanism by which pancreatic β-cells are able to alleviate cytosolic Ca²⁺ overload and its detrimental consequences.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2008년도 제49회 학술심포지움 및 국제학술대회
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• pp.90.2-90.2
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• 2008

• 대한약리학회지
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• 제32권1호
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• pp.13-21
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• 1996

세포내 칼슘농도는 신경세포의 다양한 기능에 매우 중요한 역할을 하고 있다. 본 연구에서는 일차배양한 마우스 소뇌과립세포에서 니코틴성 아세틸콜린 수용체가 특정 발생단계에 발현되고 세포내 칼슘의 농도조절에 관여하는 것을 관찰하였다. 니코틴에 의한 세포내 칼슘농도의 변화는 $^{45}Ca^{2+}$나 fura-2를 사용하여 형광법으로 측정하였다. 니코틴은 마우스 소뇌과립세포내 칼슘의 농도를 최대한 증가시키는 것으로 보인다. 반면에 일차배양한 Glia 세포들에서는 $^{45}Ca^{2+}$ 농도를 증가시키지 않았다. 세포내 칼슘농도에 미치는 니코틴의 효과는 NMDA 수용체에 대한 길항제에 의하여 억제되었다. 또한 Glutamate pyruvate transminase (GPT)를 사용하여 배양액의 글루타민산을 제거하면 니코틴효과가 소실되는 것이 관찰되었다. 이러한 결과는 니코틴에 의한 세포내 칼슘농도의 변화가 세포에서 유리된 글루타민산에 의한 간접적인 효과임을 암시한다. Fura-2를 사용한 형광법으로 실험한 결과 니코틴은 two phase로 세포내 칼슘농도를 증가시키는 것을 보여주었다. NMDA 수용체 길항제와 GPT는 단지 후기 plateau상만 억제하였다. 따라서 본 연구결과는 니코틴이 직접 니코틴성 아세틸콜린 수용체를 자극하여 일시적으로 세포내 칼슘농도를 증가시키고 글루타민산을 유리하여 NMDA 수용체를 활성화시킴으로써 세포내 칼슘농도를 지속적으로 증가시키는 것으로 보여진다. 이러한 결과는 니코틴성 아세틸콜린 수용체가 특정한 발생과정에 발현되어 세포내 칼슘농도 조절에 관여함으로써 신경발생과정에서 중요한 역할을 할 수 있음을 보여주고 있다. state를 나타내는 것을 알 수 있다. 또한 $[^3H]DPCPX$를 이용한 competitive binding assay에서 0.1 mM GTP는 효현제인 PIA의 apparent affinity를 감소시켰으며, DPCPX의 apparent affinity는 증가시키고, CGS-15943에는 아무런 영향을 미치지 않았다. 이것은 상기의 $[^{35}S]GTP_{\gamma}S$ binding의 결과를 뒤받침해 주는 결과라고 생각된다.요한 역할을 할 수 있으리라 사료된다.X>$Ca^{2+}$에 의하여 활성화되는 $K^+$ 통로를 개방시킴으로 세포내 $Ca^{2+}$을 감소시켜 뇌 기저동맥의 이완반응을 매개하는 것으로 사료된다. 함량을 조정하므로, 흉선세포의 apoptosis에 억제적으로 작용할 수 있음을 시사하는 것으로 사료된다. 영양액에 의하여는 회복됨을 볼 수 있었으며 $Mg^{++}$ 증가 영양액에서는 억제, TTX 동시 투여시에는 완전히 소실되었다. 이상의 실험결과로 흰쥐 해마에서 $A_1-adenosine$ 수용체를 통한 adenosine의 NE 유리 감소는 TEA 및 4AP에 예민한 $K^+$-통로가 관여하고 여기에는 세포외액의 Ca^{++}의 농도가 중요한 인자의 하나로 관여 하는 것으로 사료된다. 영상의 질을 크게 향상 시켜 줌으로 비가역 3구획모델에서의 PGA방법을 대체할 새로운 파라메터 영상구성방법으로 적합할 것이다.관계되며, YH439는 중금속으로 유도된 조직독성에 방어효과가 있음을 지지한다.총 아미노산의 순은

• BMB Reports
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• 제43권3호
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• pp.158-163
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• 2010

Calumenin is a multiple EF-hand $Ca^{2+}$-binding protein located in the endo/sarcoplasmic reticulum of mammalian hearts. Calumenin belongs to the CREC family of $Ca^{2+}$-binding proteins having multiple EF-hands. $Ca^{2+}$ homeostasis in the sarcoplasmic reticulum (SR) of mammalian hearts is maintained by RyR2, SERCA2 and other associated SR resident proteins. Evidence suggests that calumenin interacts with RyR2 and SERCA2, and therefore changes in the expression of calumenin could alter $Ca^{2+}$ cycling in mouse heart. In this review, current knowledge of the biochemical and functional roles of calumenin in mouse heart is described.

• Preventive Nutrition and Food Science
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• 제2권3호
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• pp.219-224
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• 1997

The pancreas is an important organ in the maintenance of zine homeostasis. The pancreatic tissue used in this study was obtained from rats fed varying levels of dietary Ca nd phytate followed by intraperitoneal {TEX}${65}^Zn${/TEX} injection. THe objective of this study was to determine the molecular size and distribution of compounds that may represent zinc-binding complexes in pancreatic tissue homogenates. The supernatant of the homogenized pancreatic tissue was separated using a Sephadex G-75 column with Tris buffer at pH 8.1. All subfractions were assayed for zinc, protein and {TEX}${65}^Zn${/TEX} activity. The elution of subfractions from pancreatic tissue homogenates showed a prominent peak corresponding to the high molecular weight protein standard (>66kd). A sall molecular weigth protein (<6.5kd), that was absorbed at 280nm, was also present: prominently in low Ca group, however not much as in high Ca group. These small compounds may combine weakly with zinc in pancreatic tissue an serve as zinc-binding ligands in pancreatic/biliary fluid. In the duodenum, these ligands dissociate zinc into an ionic form which becomes vulnerable to phytate complexation.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2001년도 한국생물과학협회 학술발표대회
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• pp.211.2-211
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• 2001

No Abstract, See Full Text

• BMB Reports
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• 제41권1호
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• pp.11-22
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• 2008

Apoptosis (programmed cell death) is a cellular self-destruction mechanism that is essential for a variety of biological events, such as developmental sculpturing, tissue homeostasis, and the removal of unwanted cells. Mitochondria play a crucial role in regulating cell death. $Ca^{2+}$ has long been recognized as a participant in apoptotic pathways. Mitochondria are known to modulate and synchronize $Ca^{2+}$ signaling. Massive accumulation of $Ca^{2+}$ in the mitochondria leads to apoptosis. The $Ca^{2+}$ dynamics of ER and mitochondria appear to be modulated by the Bcl-2 family proteins, key factors involved in apoptosis. The number and morphology of mitochondria are precisely controlled through mitochondrial fusion and fission process by numerous mitochondria-shaping proteins. Mitochondrial fission accompanies apoptotic cell death and appears to be important for progression of the apoptotic pathway. Here, we highlight and discuss the role of mitochondrial calcium handling and mitochondrial fusion and fission machinery in apoptosis.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.66-66
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• 2001

Diabetic cardiomyopathy has been suggested to be caused by abnormal intracellular $Ca^{2＋}$ homeostasis in the myocardium, which is partly due to a defect in calcium transport by the cardiac sarcoplasmic reticulum (SR). In the present study, the underlying mechanism for this functional derangement was investigated with respect to SR $Ca^{2＋}$-ATPase and phospholamban (PLB, the inhibitor of SR $Ca^{2+}$-ATPase).(omitted)d)