• The Korean Journal of Physiology and Pharmacology
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• 제22권3호
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• pp.277-289
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• 2018

The exponential increase in the use of mobile communication has triggered public concerns about the potential adverse effects of radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones on the central nervous system (CNS). In this study, we explored the relationship between calcium channels and apoptosis or autophagy in the hippocampus of C57BL/6 mice after RF-EMF exposure with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Firstly, the expression level of voltage-gated calcium channels (VGCCs), a key regulator of the entry of calcium ions into the cell, was confirmed by immunoblots. We investigated and confirmed that pan-calcium channel expression in hippocampal neurons were significantly decreased after exposure to RF-EMF. With the observed accumulation of autolysosomes in hippocampal neurons via TEM, the expressions of autophagy-related genes and proteins (e.g., LC3B-II) had significantly increased. However, down-regulation of the apoptotic pathway may contribute to the decrease in calcium channel expression, and thus lower levels of calcium in hippocampal neurons. These results suggested that exposure of RF-EMF could alter intracellular calcium homeostasis by decreasing calcium channel expression in the hippocampus; presumably by activating the autophagy pathway, while inhibiting apoptotic regulation as an adaptation process for 835 MHz RF-EMF exposure.

• BMB Reports
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• 제50권6호
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• pp.323-328
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• 2017

Lysophosphatidylcholine (LPC) is a major phospholipid component of oxidized low-density lipoprotein (ox-LDL) and is implicated in its atherogenic activity. This study investigated the effects of LPC on cell viability, intracellular calcium homeostasis, and the protective mechanisms of chlorogenic acid (CGA) in human umbilical vein endothelial cells (HUVECs). LPC increased intracellular calcium ($[Ca^{2+}]_i$) by releasing $Ca^{2+}$ from intracellular stores and via $Ca^{2+}$ influx through store-operated channels (SOCs). LPC also increased the generation of reactive oxygen species (ROS) and decreased cell viability. The mRNA expression of Transient receptor potential canonical (TRPC) channel 1 was increased significantly by LPC treatment and suppressed by CGA. CGA inhibited LPC-induced $Ca^{2+}$ influx and ROS generation, and restored cell viability. These results suggested that CGA inhibits SOC-mediated $Ca^{2+}$ influx and ROS generation by attenuating TRPC1 expression in LPC-treated HUVECs. Therefore, CGA might protect endothelial cells against LPC injury, thereby inhibiting atherosclerosis.

• 한국동물생명공학회지
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• 제36권3호
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• pp.129-136
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• 2021

This study identified single nucleotide polymorphisms (SNPs) that affect the body weight of chickens. Analysis of body weight showed that the Cornish breed had the highest body weight, and the Korean native chicken (Gray Brown) had the lowest body weight. TSH is composed of an α-subunit and a β-subunit, and the TSH-β gene encoding the β-subunit has been reported to be associated with obesity. In chickens, it is located on chromosome 26 and is reported to be associated with growth. The calcium-sensing receptor gene (CaSR) plays a role in the regulation of extracellular calcium homeostasis and is responsible for calcium absorption in the urinary tract, which affects the eggshell quality in poultry. It was shown that TSH-β was strongly correlated with weight in Cornish and Korean native (Gray Brown) chickens, particularly in those with the CC trait. However, CaSR showed no association with body weight in poultry; it was associated with calcium and the eggshell. Thus, selection for TSH-β can be used to produce individuals with more favorable traits in terms of body weight.

• 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

• Journal of Nutrition and Health
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• 제44권6호
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• pp.474-480
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• 2011

Calcium (Ca) is an essential element to maintain body homeostasis. However, many factors disturb calcium absorption. Aspartic acid chelated calcium (AAC) was synthesized by new methods using calcium carbonate and aspartic acid. This study was carried out to investigate the bioavailability of AAC in Ca-deficient rats. The experimental groups were as follows: NC; normal diet control group, CD-C; untreated control group of Ca-deficient (CD) rats, CD-$CaCO_3$; $CaCO_3$ treated group of CD rats, CD-AAC; AAC treated group of CD rats, and CD-SWC; and seaweed-derived Ca treated group of CD rats. The Ca content of various types of Ca was held constant at 32 mg/day, and the four CD groups were fed for 7 days after randomized grouping. Ca content in serum, urine, and feces within feeding periods were analyzed to confirm Ca absorption. Serum Ca content was significantly higher in the CD-AAC (11.24 mg/dL) and CD-SWC (10.12 mg/dL) groups than that in the CD-C (8.6 mg/dL) group 2 hours following the first administration. The Ca content in feces was significantly lower in the CD-AAC (35.4 mg/3 days) and CD-SWC (71.1 mg/3 day) groups than that in the CD-$CaCO_3$ (98.7 mg/3 days) group (p > 0.05). AAC had a 2.3-fold higher absorption rate of Ca than that of SWC. No differences in fibula length were observed in the NC and CD groups. The fibula weights of the CD-AAC (0.33 g) and CD-SWC (0.33 g) groups increased compared to those in the CD-C (0.27 g) group; however, no significant difference was observed between the CD groups. We conclude that bioavailability of AAC is higher than that of seaweed-derived Ca or inorganic Ca. Thus, these findings suggest the AAC has potential as a functional food material related to Ca metabolism.

• Journal of Veterinary Science
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• 제23권2호
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• pp.26.1-26.12
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• 2022

Background: Glutamate is the main excitatory neurotransmitter. Excessive glutamate causes excitatory toxicity and increases intracellular calcium, leading to neuronal death. Parvalbumin is a calcium-binding protein that regulates calcium homeostasis. Quercetin is a polyphenol found in plant and has neuroprotective effects against neurodegenerative diseases. Objectives: We investigated whether quercetin regulates apoptosis by modulating parvalbumin expression in glutamate induced neuronal damage. Methods: Glutamate was treated in hippocampal-derived cell line, and quercetin or vehicle was treated 1 h before glutamate exposure. Cells were collected for experimental procedure 24 h after glutamate treatment and intracellular calcium concentration and parvalbumin expression were examined. Parvalbumin small interfering RNA (siRNA) transfection was performed to detect the relation between parvalbumin and apoptosis. Results: Glutamate reduced cell viability and increased intracellular calcium concentration, while quercetin preserved calcium concentration and neuronal damage. Moreover, glutamate reduced parvalbumin expression and quercetin alleviated this reduction. Glutamate increased caspase-3 expression, and quercetin attenuated this increase in both parvalbumin siRNA transfected and non-transfected cells. The alleviative effect of quercetin was statistically significant in non-transfected cells. Moreover, glutamate decreased bcl-2 and increased bax expressions, while quercetin alleviated these changes. The alleviative effect of quercetin in bcl-2 family protein expression was more remarkable in non-transfected cells. Conclusions: These results demonstrate that parvalbumin contributes to the maintainace of intracellular calcium concentration and the prevention of apoptosis, and quercetin modulates parvalbumin expression in glutamate-exposed cells. Thus, these findings suggest that quercetin performs neuroprotective function against glutamate toxicity by regulating parvalbumin expression.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2003년도 춘계학술대회
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• pp.73-74
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• 2003

• Endocrinology and Metabolism
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• 제33권4호
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• pp.485-492
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• 2018

Background: Increasing evidence supports interplay between aldosterone and parathyroid hormone (PTH), which may aggravate cardiovascular complications in various heart diseases. Negative structural cardiovascular remodeling by primary aldosteronism (PA) is also suspected to be associated with changes in calcium levels. However, to date, few clinical studies have examined how changes in calcium and PTH levels influence cardiovascular outcomes in PA patients. Therefore, we investigated the impact of altered calcium homeostasis caused by excessive aldosterone on cardiovascular parameters in patients with PA. Methods: Forty-two patients (mean age $48.8{\pm}10.9$ years; 1:1, male:female) whose plasma aldosterone concentration/plasma renin activity ratio was more than 30 were selected among those who had visited Severance Hospital from 2010 to 2014. All patients underwent adrenal venous sampling with complete access to both adrenal veins. Results: The prevalence of unilateral adrenal adenoma (54.8%) was similar to that of bilateral adrenal hyperplasia. Mean serum corrected calcium level was $8.9{\pm}0.3mg/dL$ (range, 8.3 to 9.9). The corrected calcium level had a negative linear correlation with left ventricular end-diastolic diameter (LVEDD, ${\rho}=-0.424$, P=0.031). Moreover, multivariable regression analysis showed that the corrected calcium level was marginally associated with the LVEDD and corrected QT (QTc) interval (${\beta}=-0.366$, P=0.068 and ${\beta}=-0.252$, P=0.070, respectively). Conclusion: Aldosterone-mediated hypercalciuria and subsequent hypocalcemia may be partly involved in the development of cardiac remodeling as well as a prolonged QTc interval, in subjects with PA, thereby triggering deleterious effects on target organs additively.

• International Journal of Oral Biology
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• 제42권3호
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• pp.85-90
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• 2017

Mitochondria participate in various intracellular metabolic pathways such as generating intracellular ATP, synthesizing several essential molecules, regulating calcium homeostasis, and producing the cell's reactive oxygen species (ROS). Emerging studies have demonstrated newly discovered roles of mitochondria, which participate in the regulation of innate immune responses by modulating NLRP3 inflammasomes. Here, we review the recently proposed pathways to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation: 1) mitochondrial ROS, 2) calcium mobilization, 3) nicotinamide adenine dinucleotide ($NAD^+$) reduction, 4) cardiolipin, 5) mitofusin, 6) mitochondrial DNA, 7) mitochondrial antiviral signaling protein. Furthermore, we highlight the significance of mitophagy as a negative regulator of mitochondrial damage and NLRP3 inflammasome activation, as potentially helpful therapeutic approaches which could potentially address uncontrolled inflammation.

• 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.