• 생명과학회지
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• 제26권10호
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• pp.1137-1152
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• 2016

세포는 다양한 인체 질환에 관련되어 있는 저산소 환경을 인지하고 반응하며 적응한다. 저산소 상태에 적응하기 위해서는 hypoxic 유전자의 발현을 증가시키고 aerobic 유전자의 발현을 감소시키는 유전자 발현 조절이 필요하다. 최근 연구에서 미토콘드리아 호흡계가 이러한 유전자 발현 조절에 관여됨이 밝혀지고 있다. 본 연구에서는 호흡이 가능한 곰팡이(Saccharomyces cerevisiae)와 호흡이 불가능한 돌연변이 곰팡이를 실험대상으로 하여 미토콘드리아 호흡계가 저산소 환경에서 유전자 발현 조절에 관여됨을 DNA microarray 기법을 이용하여 전체 유전자를 대상으로 조사하였다. 산소 농도가 감소함에 반응하여 많은 유전자의 발현에 변화가 있었으며, 이러한 차별적인 발현 양상을 보이는 유전자는 여러 그룹으로 분류할 수 있었다. 대부분의 hypoxic 그리고 aerobic 유전자는 저산소 상태에 적응하는 발현 양상을 위해서는 미토콘드리아 호흡계가 필요하였다. 그러나 일부 hypoxic 그리고 aerobic 유전자는 미토콘드리아 호흡계와 무관하게 저산소 상태에 적응하는 발현 양상을 보였다. 이러한 결과는 미토콘드리아 호흡계가 저산소 환경에 적응하는 유전자 발현 조절에 필요하며, 또한 여러 기전을 통하여 이러한 유전자 발현 조절에 관여함을 제시한다. 또한 microarray 실험 결과에서 도출된 산소 농도에 대해 차별적인 발현을 보이는 유전자에 대하여 gene ontology 및 promoter 분석을 수행하였고 이러한 추가 분석 결과는 산소에 의해 조절되는 유전자와 함께 세포가 저산소 환경에 적응하는 기작을 이해하는 데 유용한 자료가 될 것으로 기대된다.

• 미생물학회지
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• 제19권2호
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• pp.63-77
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• 1981

The growth rate of yeast population (Saccharomyces uvarum) cultivated in the Knopp's modified medium (plus various carbon sources) appeared the highest value when the Knopp's minimal medium was treated to 1.5% with disaccharide such as maltose and sucrose. Also the treatment of lactose and raffinose resulted in polulation growth as to the population size in case of maltose and sucrose. However, the gorwth of yeast was not occurred at all when a polysaccharide, such as inulin, was added as carbon source. The growth from of yeast population in Knopp's modified medium are characterized by the fact that log phase continued 100hrs after inoculation and that stationary state phase appeared in general 250hrs after inoculation. Applying the various carbon sources to respiration substrate for yeast cell, the respiration rate of yeast showed the highest value in treatment of maltose and followed in order of raffinose, lactose, glucose, and sucrose. Determined the amount of poly-phosphate and turn over pathway of poly-phosphate according to culture phase of yeast, it is revealed that the yeast synthesized 3 types of poly phosphate (poly-P A,B, and C) and postulated that turn over pathway of poly-phosphate as follows ; Inorganic phosphate is converted into each kind of polyphosphates, and then one part of poly-P-C is converted into poly-P-B, the rest poly-p-C and poly-P-B are converted into poly-P-A. The synthesized poly-phosphate is considered to have a role as energy pool utilizing to synthesis of cellular organic materials. Of the 13 carbon sources used in this experiment, the useful carbon sources for biosynthesis of poly-phosphate and cellular organic materials are confirmed as disaccharide (maltose and sucrose) as well as glucose. Protein synthesis in yeast cell showed the two peaks on 6th and 8th day after inoculation ; nucleic acid on 2nd day (48hrs), carbohydrates on 2nd day (48hrs), and phospholipid on 2nd and 8th day after inoculation, respectively.

• 센서학회지
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• 제25권1호
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• pp.51-56
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• 2016

This study evaluates the performance of an optical sensor and measurement system (CMA-24) which can analyze the fluctuation of dissolved oxygen and pH simultaneously. In the optical sensor system, the fluorescent materials, Rudpp and HPTS which are sensitive to dissolved oxygen and pH, respectively, are coated on the bottom of a 24-well -plate by the sol-gel technology. The detection times of the emission light of the oxygen sensor were $4,186{\pm}13.90{\mu}s$ and $4,452{\pm}36.68{\mu}s$ for the dissolved oxygen of 17% $O_2$ and 7.6% $O_2$, respectively. On the other hand, the detection times of the pH sensor were $6,699.43{\pm}14.64{\mu}s$, $6,722.24{\pm}6.21{\mu}s$, and $6,748.52{\pm}2.63{\mu}s$ using pH 6, 7, and 8, respectively. When we determined cellular respiration levels of C2C12 myocytes with CMA-24, $O_2$/pH measurement system, the ratio of the uncoupled to coupled OCR (oxygen consumption rate) was 1.41. The results mean that this CMA-24 system shows almost the same sensitiveness as the commercial system.

• Asian Pacific Journal of Cancer Prevention
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• 제15권4호
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• pp.1711-1714
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• 2014

Objective: To explore the effect of Withaferin A on A549 cellular proliferation and apoptosis in non-small cell lung cancer (NSCLC). Materials and Methods: NSCLC cell line A549 was selected to explore the effect of Withaferin A on A549 cellular proliferation, apoptosis and the PI3K/Akt signal pathway capable of regulating tumor biological behavior by assessment of cellular proliferation, cellular apoptotic rates and cellular cycling as well as by immuno-blotting. Results: Withaferin A could inhibit A549 cellular proliferation and the control rate was dosage-dependent (P<0.05), which also increased time-dependently with the same dosage of Withaferin A (P<0.05). The apoptotic indexes in A549 cells treated with 0, 2.5, 5.0, 10.0 and 20.0 ${\mu}mol{\cdot}L^{-1}$ Withaferin A for 48 h were significantly different (P<0.05). In addition, the apoptotic rates of each group in both early and advanced stages were higher than those in 0 ${\mu}mol{\cdot}L^{-1}$ (P<0.05), which were evidently higher after 48 h than those after 24 h (P<0.05). A549 cells treated by Withaferin A for 48 h were markedly lower in Bcl-2 level and obviously higher in Bax and cleaved caspase-3 levels than those treated by 0 ${\mu}mol{\cdot}L^{-1}$ Withaferin A (P<0.05), and there were significant differences among 5, 10 and 20 ${\mu}mol{\cdot}L^{-1}$ Withaferin A (P<0.05). The ratios of A549 cells treated by Withaferin A for 48 h in G0/G1 stage were higher than those in 0 ${\mu}mol{\cdot}L^{-1}$, while those in S and G2/M stages were obviously lower than those in G2/M stage, and there were significant differences in 5.0, 10.0 and 20.0 ${\mu}mol{\cdot}L^{-1}$ Withaferin A (P<0.05). Additionally, p-Akt/Akt values were in reverse association with dosage, and the differences were significant (P<0.05). Conclusion: Withaferin A can inhibit the proliferation and apoptosis of A549 cells by suppressing activation of the PI3K/Akt pathways.

• The Korean Journal of Physiology
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• 제30권1호
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• pp.105-116
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• 1996

Rendering the brain ischemic would evoke the cerebral ischemic reflex which is characterized by an arterial pressor response, apnea and bradycardia. Since the rostral ventrolateral medulla (RVLM) is known to play a key role in the maintenance of normal cardiopulmonary activity, during the cerebral ischemic reflex some cardiac related cells should be excited and respiration related cells inhibited. In this context, the responses of RVLM neurons to systemie and focal hypoxia were analyzed in the present study. Twenty-five adult cats of either sex were anesthetized with ${\alpha}-chloralose$ and the single neuronal activities were identified from RVLM area. For the induction of focal hypoxia in the recording site, sodium cyanide was applied iontophoretically and for systemic hypoxia the animal was ventilated with nitrogen gas for a twenty-second period. Cellular activities were analyzed in terms of their discharge pattern and responses to the hypoxia by using post-stimulus time and single-pass time histograms. Of eighteen cardiac related cells recorded from the RVLM area, twelve cells were excited by iontophoresed sodium cyanide and of twenty-five respiration related cells, fourteen cells were excited by iontophoresed sodium cyanide. Remaining cells were either inhibited or unaffected. Eight of fifteen cells tested with iontophoresed sodium lactate were excited and remaining seven cells were inhibited. Systemic hypoxia induced by nitrogen gas inhalation elevated the arterial blood pressure, but excited, inhibited or unaffected the single neuronal activities. Some cells showed initial excitation followed by inhibition during the systemic hypoxia. Bilateral vagotomy resulted in a decrease of arterial pressor response to the systemic hypoxia, and a slight decrease in the rhythmicity related to cardiac and/or respiratory rhythms. The single neuronal responses to either systemic or focal hypoxia were not affected qualitatively by vagotomy. From the above results, it was concluded that the majority of the cardiac- and respiration- related neurons in the rostral ventrolateral medulla be excited by hypoxia, not through the mediation of peripheral chemoreceptors, and along with the remaining inhibited cells, all these cells be involved in the mediation of cerebral ischemic reflex.

• Molecular & Cellular Toxicology
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• 제4권1호
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• pp.45-51
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• 2008

Volatile Organic Compounds (VOCs) have been shown to cause nervous system disorders through skin contact or respiration, and also cause foul odors even at low densities in most cases. Also, as a compound itself, VOCs are directly harmful to the environment and to the human body, and may participate in photochemical reactions in air to create secondary pollutants. In this study, HL-60 cells were treated with volatile organic compounds, including ethylbenzene and trichloroethylene, at a value of $IC_50$. Then, the in house-prepared Human HazChem arrayer was utilized in order to compare the gene expression between the two VOCs. After hybridization, 8 upregulated genes and 8 downregulated genes were discovered in the HazChem array. The upregulated genes were identified as SG15, TNFSF10, PRNP, ME1, NCOA4, SRXN1, TXNRD1, and XBP1. The downregulated genes were identified as MME, NRF1, PRARBP, CALCA, CRP, BAX, C7 or f40, and FGFR1. Such results were highly correlated with the quantitative RT-PCR results. The majority of the 16 genes were related with the characteristics of VOCs, including respiratory mechanism, apoptosis, and carcinogenesis-associated genes. Our data showed that our human HazChem array can be used to monitor hazardous materials via gene expression profiling.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.567-577
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• 2017

Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in $O_2$ respiration and increase in oxidative stress) in skeletal muscle. The balance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mitochondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal muscle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle.

• BMB Reports
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• 제56권2호
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• pp.49-55
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• 2023

Aging is characterized by a gradual decline in biological functions, leading to the increased probability of diseases and deaths in organisms. Previous studies have identified biological factors that modulate aging and lifespan, including non-coding RNAs (ncRNAs). Here, we review the relationship between aging and tRNA-derived small RNAs (tsRNAs), ncRNAs that are generated from the cleavage of tRNAs. We describe age-dependent changes in tsRNA levels and their functions in age-related diseases, such as cancer and neurodegenerative diseases. We also discuss the association of tsRNAs with aging-regulating processes, including mitochondrial respiration and reduced mRNA translation. We cover recent findings regarding the potential roles of tsRNAs in cellular senescence, a major cause of organismal aging. Overall, our review will provide useful information for understanding the roles of tsRNAs in aging and age-associated diseases.

• The Plant Pathology Journal
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• 제40권2호
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• pp.99-105
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• 2024

Land plants produce glucose (C₆H₁₂O₂) through photosynthesis by utilizing carbon dioxide (CO₂), water (H₂O), and light energy. Glucose can be stored in various polysaccharide forms for later use (e.g., sucrose in fruit, amylose in plastids), used to create cellulose, the primary structural component of cell walls, and immediately metabolized to generate cellular energy, adenosine triphosphate, through a series of respiratory pathways including glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation. Additionally, plants must metabolize glucose into amino acids, nucleotides, and various plant hormones, which are crucial for regulating many aspects of plant physiology. This review will summarize the biosynthesis of different plant hormones, such as auxin, salicylic acid, gibberellins, cytokinins, ethylene, and abscisic acid, in relation to glucose metabolism.

• Journal of Ginseng Research
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• 제45권4호
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• pp.473-481
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• 2021

Background: Mitochondrial dysfunction is one of the significant reasons for Alzheimer's disease (AD). Ginsenosides, natural molecules extracted from Panax ginseng, have been demonstrated to exert essential neuroprotective functions, which can ascribe to its anti-oxidative effect, enhancing central metabolism and improving mitochondrial function. However, a comprehensive analysis of cellular mitochondrial bioenergetics after ginsenoside treatment under Aβ-oxidative stress is missing. Methods: The antioxidant activities of ginsenoside Rb₁, Rd, Re, Rg₁ were compared by measuring the cell survival and reactive oxygen species (ROS) formation. Next, the protective effects of ginsenosides of mitochondrial bioenergetics were examined by measuring oxygen consumption rate (OCR) in PC12 cells under Aβ-oxidative stress with an extracellular flux analyzer. Meanwhile, mitochondrial membrane potential (MMP) and mitochondrial dynamics were evaluated by confocal laser scanning microscopy. Results: Ginsenoside Rg₁ possessed the strongest anti-oxidative property, and which therefore provided the best protective function to PC12 cells under the Aβ oxidative stress by increasing ATP production to 3 folds, spare capacity to 2 folds, maximal respiration to 2 folds and non-mitochondrial respiration to 1.5 folds, as compared to Aβ cell model. Furthermore, ginsenoside Rg1 enhanced MMP and mitochondrial interconnectivity, and simultaneously reduced mitochondrial circularity. Conclusion: In the present study, these results demonstrated that ginsenoside Rg₁ could be the best natural compound, as compared with other ginsenosides, by modulating the OCR of cultured PC12 cells during oxidative phosphorylation, in regulating MMP and in improving mitochondria dynamics under Aβ-induced oxidative stress.