• Title/Summary/Keyword: epithelial

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New Isolation Technique and Culture System for Clinical Applications of Human Amniotic Epithelial Stem Cells (인간태반양막유래 상피줄기세포의 임상적용을 위한 새로운 세포분리 및 배양 기술)

  • Woo, Sang-Kyu;Jo, Jung-Yoon;Shin, Il-Seob;Kang, Sung-Keun;Ra, Jeong-Chan
    • Development and Reproduction
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    • v.13 no.4
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    • pp.271-280
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    • 2009
  • Human placenta is abundant source of adult stem cells. Especially, amniotic epithelial cells have stem cell characteristics, expressing surface markers normally present on embryonic stem cells and germ cells. However, culturing and expanding amniotic epithelial cells in vitro without feeder cells are difficult due to endogenous characteristics of epithelial cells. In the present study, amniotic epithelial cells are isolated and proliferated in several passages by applying dithiothreitol and a Rho-associated kinase inhibitor in culture media. The cultured amniotic epithelial cells showed the epithelial and stem cell characteristics. In conclusion, human placenta-derived amniotic epithelial stem cells can be a major source of stem cells for medical treatment of various diseases without any controversial issues.

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Inhibitory effect of Korean Red Ginseng extract on DNA damage response and apoptosis in Helicobacter pylori-infected gastric epithelial cells

  • Kang, Hyunju;Lim, Joo Weon;Kim, Hyeyoung
    • Journal of Ginseng Research
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    • v.44 no.1
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    • pp.79-85
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    • 2020
  • Background: Helicobacter pylori increases reactive oxygen species (ROS) and induces oxidative DNA damage and apoptosis in gastric epithelial cells. DNA damage activates DNA damage response (DDR) which includes ataxia-telangiectasia-mutated (ATM) activation. ATM increases alternative reading frame (ARF) but decreases mouse double minute 2 (Mdm2). Because p53 interacts with Mdm2, H. pylori-induced loss of Mdm2 stabilizes p53 and induces apoptosis. Previous study showed that Korean Red Ginseng extract (KRG) reduces ROS and prevents cell death in H. pylori-infected gastric epithelial cells. Methods: We determined whether KRG inhibits apoptosis by suppressing DDRs and apoptotic indices in H. pylori-infected gastric epithelial AGS cells. The infected cells were treated with or without KRG or an ATM kinase inhibitor KU-55933. ROS levels, apoptotic indices (cell death, DNA fragmentation, Bax/Bcl-2 ratio, caspase-3 activity) and DDRs (activation and levels of ATM, checkpoint kinase 2, Mdm2, ARF, and p53) were determined. Results: H. pylori induced apoptosis by increasing apoptotic indices and ROS levels. H. pylori activated DDRs (increased p-ATM, p-checkpoint kinase 2, ARF, p-p53, and p53, but decreased Mdm2) in gastric epithelial cells. KRG reduced ROS and inhibited increase in apoptotic indices and DDRs in H. pylori-infected gastric epithelial cells. KU-55933 suppressed DDRs and apoptosis in H. pylori-infected gastric epithelial cells, similar to KRG. Conclusion: KRG suppressed ATM-mediated DDRs and apoptosis by reducing ROS in H. pylori-infected gastric epithelial cells. Supplementation with KRG may prevent the oxidative stress-mediated gastric impairment associated with H. pylori infection.

Contributions of HO-1-Dependent MAPK to Regulating Intestinal Barrier Disruption

  • Zhang, Zhenling;Zhang, Qiuping;Li, Fang;Xin, Yi;Duan, Zhijun
    • Biomolecules & Therapeutics
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    • v.29 no.2
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    • pp.175-183
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    • 2021
  • The mitogen-activated protein kinase (MAPK) pathway controls intestinal epithelial barrier permeability by regulating tight junctions (TJs) and epithelial cells damage. Heme oxygenase-1 (HO-1) and carbon monoxide (CO) protect the intestinal epithelial barrier function, but the molecular mechanism is not yet clarified. MAPK activation and barrier permeability were studied using monolayers of Caco-2 cells treated with tissue necrosis factor α (TNF-α) transfected with FUGW-HO-1 or pLKO.1-sh-HO-1 plasmid. Intestinal mucosal barrier permeability and MAPK activation were also investigated using carbon tetrachloride (CCl4) administration with CoPP (a HO-1 inducer), ZnPP (a HO-1 inhibitor), CO releasing molecule 2 (CORM-2), or inactived-CORM-2-treated wild-type mice and mice with HO-1 deficiency in intestinal epithelial cells. TNF-α increased epithelial TJ disruption and cleaved caspase-3 expression, induced ERK, p38, and JNK phosphorylation. In addition, HO-1 blocked TNF-α-induced increase in epithelial TJs disruption, cleaved caspase-3 expression, as well as ERK, p38, and JNK phosphorylation in an HO-1-dependent manner. CoPP and CORM-2 directly ameliorated intestinal mucosal injury, attenuated TJ disruption and cleaved caspase-3 expression, and inhibited epithelial ERK, p38, and JNK phosphorylation after chronic CCl4 injection. Conversely, ZnPP completely reversed these effects. Furthermore, mice with intestinal epithelial HO-1 deficient exhibited a robust increase in mucosal TJs disruption, cleaved caspase-3 expression, and MAPKs activation as compared to the control group mice. These data demonstrated that HO-1-dependent MAPK signaling inhibition preserves the intestinal mucosal barrier integrity by abrogating TJ dysregulation and epithelial cell damage. The differential targeting of gut HO-1-MAPK axis leads to improved intestinal disease therapy.

Effects of Hantaan Virus and $IFN-{\gamma}$ on Induction of Surface ICAM-1 in Primary Cultured Human Nasal Epithelial Cells and Human Lung Fibroblasts

  • Park, Ho-Sun;Kim, Sung-Kwang
    • The Journal of Korean Society of Virology
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    • v.28 no.4
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    • pp.317-325
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    • 1998
  • The primary culture of human nasal epithelial cells was performed using the inferior nasal turbinate tissues, and infected with Hantaan virus to examine the hypothesis of airborne transmission of Hantaan virus in humans. The primary culture cells were identified as epithelial cells by morphologic and immunologic analyses. The viral antigens were detected in the primary human nasal epithelial cells infected with Hantaan virus by immunofluorescence staining. The ICAM-1 induction by Hantaan virus or $IFN-{\gamma}$ was examined in the primary human nasal epithelial cells and human lung fibroblasts (WI-38). Hantaan virus induced the surface ICAM-1 in WI-38 cells in a time-dependent manner, and $IFN-{\gamma}$ induced the surface ICAM-1 in a dose-dependent manner in HNEC and WI-38 cells. These results revealed that the human nasal epithelial cells are susceptible to Hantaan viral infection supporting the hypothesis of airborne transmission of Hantaan virus in humans. The human lung fibroblasts also might have an important role in the pathogenesis of Hantaan virus through the induction of ICAM-1.

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CLINICAL TREATMENT AND PROGNOSIS OF EPITHELIAL DYSPLASIA IN HISTOPATHOLOGIC FINDINGS;CASE REPORTS (조직병리학적으로 진단된 상피 이형성증의 임상적 치료 및 예후;증례보고)

  • Kim, Su-Kwan;Yeo, Hwan-Ho;Kim, Young-Kyun;Park, In-Soon
    • Maxillofacial Plastic and Reconstructive Surgery
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    • v.17 no.4
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    • pp.407-414
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    • 1995
  • The information concerning epithelial dysplasia of the oral cavity has been relatively little published. Of the histolgic grades, most of the cases were classified as moderate and severe category. Their ages ranged from 27 to 78 years(mean 57 years). The developmental incidence by sex was superior in male by ratio of 6 : 1. Epithelial lesions were located in the buccal mucosa, Floor of the mouth, the gingiva and the tongue. It is generally believed with a few exceptions that mild degree of epithelial dysplasia do not indicate any great danger for the patient. But severs dysplasia indicates that there is a very considerable risR of malignant transformation. Surgical excision is the effective method of controlling epithelial dysplasia. The authors investigated 7 cases of epithelial dysplasia histopathologically, 2 patients of them had malignant transformation. We discuss the clinical feature, treatment, prognosis, and histopatholgic analysis with literature reviews.

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Involvement of Cathepsin D in Apoptosis of Mammary Epithelial Cells

  • Seol, M.B.;Bong, J.J.;Baik, M.
    • Asian-Australasian Journal of Animal Sciences
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    • v.19 no.8
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    • pp.1100-1105
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    • 2006
  • During involution of the mammary gland after the lactation period, the gland undergoes an extensive epithelial cell death. In our previous study, overexpression of an extracellular proteinase inhibitor (Expi) gene accelerated apoptosis of mammary epithelial cells. Here we found that expression of the cathepsin D gene was induced in the Expi-overexpressed apoptotic cells. To understand the role of cathepsin D in apoptosis, we transfected cathepsin D gene into mammary epithelial HC11 cells and established the stable cell lines overexpressing the cathepsin D gene. We found that overexpression of the cathepsin D gene partially induced apoptosis of mammary epithelial cells. Expression patterns of the cathepsin D gene were examined in mouse mammary gland at various reproductive stages. Expression of the cathepsin D gene was increased during involution stages compared to lactation stages, and highest expression levels were shown at involution on day 4. We also examined expression of the cathepsin D gene in various mouse tissues. Mammary gland at involution on day 2 showed highest levels of cathepsin D mRNA of the mouse tissues that we examined. Liver tissues showed high levels of cathepsin D expression. These results demonstrate that cathepsin D may contribute to the apoptotic process of mammary epithelial cells.

Physiological understanding of host-microbial pathogen interactions in the gut

  • Lee, Sei-Jung;Choi, Sang Ho;Han, Ho Jae
    • Korean Journal of Veterinary Research
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    • v.56 no.2
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    • pp.57-66
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    • 2016
  • The gut epithelial barrier, which is composed of the mucosal layer and the intestinal epithelium, has multiple defense mechanisms and interconnected regulatory mechanisms against enteric microbial pathogens. However, many bacterial pathogens have highly evolved infectious stratagems that manipulate mucin production, epithelial cell-cell junctions, cell death, and cell turnover to promote their replication and pathogenicity in the gut epithelial barrier. In this review, we focus on current knowledge about how bacterial pathogens regulate mucin levels to circumvent the epithelial mucus barrier and target cell-cell junctions to invade deeper tissues and increase their colonization. We also describe how bacterial pathogens manipulate various modes of epithelial cell death to facilitate bacterial dissemination and virulence effects. Finally, we discuss recent investigating how bacterial pathogens regulate epithelial cell turnover and intestinal stem cell populations to modulate intestinal epithelium homeostasis.

Percutaneous Fine Needle Aspiration Cytology of Thymoma (흉선종의 경피 세침흡인 세포학적 검색)

  • Park, Weon-Seo;Park, In-Ae;Ham, Eui-Keun;Lee, Sang-Kook
    • The Korean Journal of Cytopathology
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    • v.4 no.1
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    • pp.16-24
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    • 1993
  • The fine needle aspiration (FNA) cytologic findings in 16 cases of histologically confirmed thymoma are reported. The aspirates were obtained under fluoroscopic guidance. The cytologic diagnoses were inadequate sample in one case, thymoma in 12(75%), small cell carcinoma or thymoma in 1, benign mesenchymal tumor in 1, and germ cell tumor in one. The cytologic features were detailed according to the constituent epithelial cell type, and into 4 small of epithelial cells and lymphocytes. Fifteen cases were classified into 4 small epithelial cell type, 6 intermediate epithelial cell type, 1 large epithelial cell type, 1 large pleomorphic epithelial cell type, and 3 spindle-shaped epithelial ceil type. Cytologic differential diagnosis was discussed, and the important criteria for the cytologic diagnosis of thymoma were reviewed. This review leads us to think that nonoperative cytologic approaches in the diagnosis of the thymoma are possible, and that correct cytologic diagnosis of thymoma with FNAs can easily be made, if adequate samples are obtained However the invasiveness and histologic type could not be predicted by cytological features only. Knowing various cytologic and histologic features of thymoma will be helpful for the diagnosis of thymoma and the differential diagnosis of modiastinal tumors.

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The Role of the Epithelial Cell in Bronchial Asthma (천식에서 기도 상피세포의 역할)

  • Chung, Jin-Hong
    • Journal of Yeungnam Medical Science
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    • v.16 no.1
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    • pp.15-24
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    • 1999
  • Although traditionally viewed as a physical barrier between the host and a variety of inhaled irritants and pathogens, it has become clear that the epithelium has a much broader functional scope. Epithelial cells arc metabolically active and can play an important role in the regulation of the allergic inflammatory response. This review provides a consideration of the role of the epithelial cell as both a "target" for exogenous and endogenous stimuli and as an "effector" cell that is capable of producing a variety of products that can influence the inflammatory response in the airways.

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Epithelial-Myoepithelial Carcinoma of the Lung; one case report (폐의 상피-근상피세포암)

  • 조성우;지현근;이재진;신윤철;남은숙
    • Journal of Chest Surgery
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    • v.33 no.6
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    • pp.518-520
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    • 2000
  • Epithelial-myoepithelial carcinoma is a rate low-grade malignant salivary neoplasm that usually occurs in the parotid gland but can also arise in minor salivary glands. We report a case of a primary epithelial-myoepithelial carcinoma of the lung neoplasm. The patient was 48-year-old women who presented with dry cough of 1 month duration. A right middle lobe endobronchial lesion was identified bronchoscopically. The bilobectomy of RML & RLL was performed, the pathologic result was epithelial-myoepithelial carcinoma.

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