• Bulletin of the Korean Chemical Society
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• 제30권6호
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• pp.1357-1359
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• 2009

Many researchers studied cell culturing on surfaces with chemical functional groups. Previously, we reported surface properties of plasma polymerized ethylenediamine (PPEDA) films deposited by plasma enhanced chemical vapor deposition with various plasma conditions. Surface properties of PPEDA films can be controlled by plasma power during deposition. In this work, to analyze correlation of cell adherence/proliferation with surface property, we cultured rat intestinal epithelial cells-18 on the PPEDA films deposited with various plasma powers. It was shown that as plasma power was decreased, density of cells cultured on the PPEDA film surface was increased. Our findings indicate that plasma power changed the amine density of the PPEDA film surface, resulting in density change of cells cultured on the PPEDA film surface.

• Tuberculosis and Respiratory Diseases
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• 제78권4호
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• pp.428-431
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• 2015

Epithelial-myoepithelial carcinoma (EMC) of lung is a minor subset of salivary type carcinoma of lung of known low grade malignancy. Histologically, two-cell components forming duct-like structure with inner epithelial cell layer and outer myoepithelial cell layer are characteristics of EMC. In salivary gland, dedifferentiation of conventional low grade malignancy has been reported and is thought to be related with poor prognosis. However, precise histomorphology and prognostic factors of pulmonary EMC have not been clarified due to its rarity. Herein, we reported a rare case of EMC presented as endobronchial mass in a 53-year old woman, which showed predominant solid lobular growth pattern and lymph node metastases.

• Journal of Microbiology and Biotechnology
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• 제29권10호
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• pp.1675-1681
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• 2019

Clostridium difficile toxin A is known to cause colonic epithelial cell apoptosis, which is considered the main causative event that triggers inflammatory responses in the colon, reflecting the concept that the essential role of epithelial cells in the colon is to form a physical barrier in the gut. We previously showed that toxin A-induced colonocyte apoptosis and subsequent inflammation were dependent on prostaglandin E2 ($PGE_2$) produced in response to toxin A stimulation. However, the molecular mechanism by which $PGE_2$ mediates cell apoptosis in toxin A-exposed colonocytes has remained unclear. Here, we sought to identify the signaling pathway involved in toxin A-induced, $PGE_2$-mediated colonocyte apoptosis. In non-transformed NCM460 human colonocytes, toxin A exposure strongly upregulated expression of Bak, which is known to form mitochondrial outer membrane pores, resulting in apoptosis. RT-PCR analyses revealed that this increase in Bak expression was attributable to toxin A-induced transcriptional upregulation. We also found that toxin A upregulation of Bak expression was dependent on $PGE_2$ production, and further showed that this effect was recapitulated by an Prostaglandin E2(PGE2) receptor-1 receptor agonist, but not by agonists of other EP receptors. Collectively, these results suggest that toxin A-induced cell apoptosis involves $PGE_2$-upregulation of Bak through the EP1 receptor.

• 한국발생생물학회지:발생과생식
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• 제26권4호
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• pp.155-163
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• 2022

Human pluripotent stem cells (hPSCs) can give rise to a vast array of differentiated derivatives, which have gained great attention in the field of in vitro toxicity evaluation. We have previously demonstrated that hPSC-derived alveolar epithelial cells (AECs) are phenotypically and functionally similar to primary AECs and could be more biologically relevant alternatives for assessing the potential toxic materials including in fine dust and cigarette smoking. Therefore, in this study, we employed hPSC-AECs to evaluate their responses to exposure of various concentrations of diesel particulate matter (dPM), cigarette smoke extract (CSE) and nicotine for 48 hrs in terms of cell death, inflammation, and oxidative stress. We found that all of these toxic materials significantly upregulated the transcription of pro-inflammatory cytokines such as IL-1α, IL-β, IL-6, and TNF-α. Furthermore, the exposure of dPM (100 ㎍/mL) strongly induced upregulation of genes related with cell death, inflammation, and oxidative stress compared with other concentrations of CSE and nicotine. These results suggest that hPSC-AECs could be a robust in vitro platform to evaluate pulmotoxicity of various air pollutants and harmful chemicals.

• 한국동물학회지
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• 제25권1호
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• pp.9-28
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• 1982

Guinea pig의 發情週期를 發情前期, 發情期, 發情後期, 그리고 發情間期의 4단계로 구분하여 子宮內膜의 表層上皮細胞에 있어서의 미세구조상의 변화와 이 세포들의 acid phosphatase, alkaline phosphatase 그리고 adenosine triphosphatase의 활성의 변화를 細胞化學的인 방법에 의하여 관찰하였고 발정주기에 따른 자궁내막표층상피세포 표면의 미세구조 변화를 走査電子顯微鏡으로 관찰하여 다음과 같은 결과를 얻었다. 1. 表層上皮細胞들은 발정기와 발정간기에서 單層圓柱形이며 발정기와 발정후기에서는 多列上皮組織으로 관찰되었고 발정전기에서 핵과 세포질의 비율이 크고 발정기에서는 세포와 핵들이 신장된 형태를 보이며 세포질이 증가하여 세포질이 子宮腔에 돌출된 모습이 관찰된 반면 발정후기와 발정간기에서는 세포의 길이가 작아졌다. 2. 細胞質내의 세포기관들은 발정기에서 미토콘드리아 및 유리리보좀의 증가와 粗面小胞多層版 構造物, 脂肪適, 리소조옴들이 다수 출현하였다. 3. 走査電子顯微鏡에 의한 연구로써 발정전기와 발정기에서 자궁내막의 표층상피세포들의 표면 미세구조는 세포의 境界가 뚜렷하였으며 특히 발정기에서는 多角形의 세포가 규칙적인 배열을 보였고 세포표면이 자궁강에 돌출된 구조를 나타냈으며, 발정후기와 발정간기의 표면은 편편하며 세포의 경계가 뚜렷하지 못하였다. 4. 微細絨毛는 발정기에서 가장 조밀하고 길게 發達된 반면에 발정후기와 발정간기에서는 짧은 미세융모가 관찰되고 數적인 면에서 감소된 경향을 보였다. 5. 전자현미경에 의한 효소활성의 관찰 결과 acid phosphatase는 발정후기에서 미세융모와 공포, alkaline phosphatase는 발정후기때 미세융모, 세포표면, 그리고 측면세포막에 매우 높은 활성을 나타내며 ATPase의 경우 발정전기와 발정기에서 미세융모와 세포막에 높은 활성을 보였다

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.80-104
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• 1996

The development of routine techniques for the isolation and in vitro maintenance of conducting airway epithelial cells in a differentiated state provides an ideal model to study the factors involved in the regulation of the expression of mucocilicary differentiation. Several key factors and conditions have been identified. These factors and conditions include the use of biphasic culture technique to achieve mucociliary differentiation and the use of such stimulators, the thickness of collagen gel substratum, the calcium level, and vitamin A, and such inhibitors, the growth factors EGF and insulin, and steroid hormones, for mucous cell differentiation. Using the defined culture medium, the life cycle of the mucous cell population in vitro was investigated. It was demonstrated that the majority of the mucous cell population in primary cultures is not involved in DNA replication. However, the mucous cell type is capable of self-renewal in culture and this reproduction is vitamin A dependent. furthermore, differentiation from non-mucous cell type to mucous cell type can be demonstrated by adding back a positive regulator such as vitamin A to the “starved” culture. Cell kinetics data suggest that vitamin A-dependent mucous cell differentiation in culture is a DNA replication-independent process and the process is inhibited by TGF-${\beta}$1.

• 치위생과학회지
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• 제17권5호
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• pp.433-438
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• 2017

Relative to its incidence, oral cancer has serious negative social effects. The exact causes of oral cancer have not been clarified, but many studies have implicated smoking and drinking. However, the fundamental mechanism of oral cancer causation has yet to be elucidated. Lysophosphatidic acid (LPA) augments epithelial mesenchymal transition (EMT) and development of various cancer cells. However, a detailed mechanistic explanation for LPA-induced EMT and the effects of EMT-promoting conditions on oral squamous cell carcinoma development remain elusive. In the present study, a quantitative reverse transcription polymerase chain reaction was used to analyze TWIST1, Slug, E-cadherin, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcript expression. Immunoblotting was used to analyze TWIST1, Slug, E-cadherin, and GAPDH protein expression. siRNAs were used to silence TWIST1 and Slug transcript expression. A matrigel-coated in vitro invasion insert was used to analyze oral cancer cell invasion. The results of the present study show that the expression levels of TWIST1 and Slug, which are EMT factors, were increased by LPA treatment in YD-10B oral squamous cell carcinoma. Conversely, E-cadherin expression was significantly reduced. In addition, transfection of the cells with TWIST1 and Slug siRNA strongly inhibited LPA-induced oral cancer cell invasion. The present study shows that TWIST1 and Slug mediate LPA-induced oral cancer cell EMT and invasiveness. The present study confirmed the mechanism by which LPA promotes oral cancer cell development, with TWIST1 and Slug providing novel biomarkers and promising therapeutic targets for oral cancer cell development.

• International Journal of Industrial Entomology and Biomaterials
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• 제47권2호
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• pp.90-98
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• 2023

The human eye, constantly exposed to solar radiation, can be damaged by UV radiation. In particular, ultraviolet B (UVB)-induced damage plays an important role in retinal degeneration and cell aging. In this study, we investigated the protective effects of the methanol extract of Oxya chinensis sinuosa (OCM), an edible insect known for its high protein content (64.2%), and various pharmacological effects, on human retinal pigment epithelial cells. ARPE-19 cells were treated with OCM and subsequently UVB irradiated. Our results showed that OCM effectively attenuates UVB-induced cell damage by reducing MAPK phosphorylation (JNK and p38 MAPK). Additionally, OCM increased the phosphorylation of Akt, and cell cycle regulators, including p21 and p27, in a dose-dependent manner. Moreover, OCM treatment increased ARPE-19 cell proliferation by activating the S6K1/S6 pathway. This study suggests that OCM prevents UVB-induced retinal cell damage by increasing cell proliferation via ROS reduction, suggesting its potential as a functional therapeutic superfood against retinal cell damage.

• Asian-Australasian Journal of Animal Sciences
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• 제18권12호
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• pp.1741-1745
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• 2005

Zinc is a trace element that is associated with a stimulation of immune function and regulation of ion balance for livestock production. In this study, the effect of zinc as inhibitor to apoptosis-induced cells was examined in vitro using mammary epithelial cell line, HC11 and macrophage cell line, NCTC3749. Cell viability, measured by MTT assay, indicated that 10 g/ml of zinc had a negative impact on cellular activity and 50 ng/ml was chosen for further testing. Apoptosis was induced in cells treated with C2-ceramide in serum-free media. DNA fragmentation and gene expression of acidic sphingomyelinase (a gene responsible for the progress of apoptosis) were distinctively low in zinc treated cells compared with those in non-treated controls. In conclusion, zinc is involved in the regulation of cell proliferation and apoptosis in mammary epithelial cells and macrophages.

• Asian Pacific Journal of Cancer Prevention
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• 제16권9호
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• pp.4137-4142
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• 2015

The zinc finger transcription factor EGR 1 has a role in controlling synaptic plasticity, wound repair, female reproductive capacity, inflammation, growth control, apoptosis and tumor progression. Recent studies mainly focused on its role in growth control and apoptosis, however, little is known about its role in epithelial-mesenchymal transition (EMT). Here, we aim to explore whether EGR 1 is involved in TGF-${\beta}1$-induced EMT in non-smallcell lung cancer cells. Transforming growth factor (TGF)-${\beta}1$ was utilized to induce EMT in this study. Western blotting, RT-PCR, and transwell chambers were used to identify phenotype changes. Western blotting was also used to observe changes of the expression of EGR 1. The lentivirus-mediated EGR 1 vector was used to increase EGR 1 expression. We investigated the change of migration to evaluate the effect of EGR 1 on non-small-cell lung cancer cells migration by transwell chambers. After stimulating with TGF-${\beta}1$, almost all A549 cells and Luca 1 cells (Non-small-cell lung cancer primary cells) changed to mesenchymal phenotype and acquired more migration capabilities. These cells also had lower EGR 1 protein expression. Overexpression of EGR 1 gene with EGR 1 vector could decrease tumor cell migration capabilities significantly after adding TGF-${\beta}1$. These data s howed an important role of EGR 1 in the EMT of non-small-cell lung cancer cells, as well as migration.