• 제목/요약/키워드: epithelial

검색결과 3,275건 처리시간 0.028초

The Epithelial-Mesenchymal Transition During Tooth Root Development

  • Kang, Jee-Hae;Park, Jin-Ho;Moon, Yeon-Hee;Moon, Jung-Sun;Kim, Sun-Hun;Kim, Min-Seok
    • International Journal of Oral Biology
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    • 제36권3호
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    • pp.135-141
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    • 2011
  • Hertwig's epithelial root sheath (HERS) consists of bi-layered cells derived from the inner and outer dental epithelia and plays important roles in tooth root formation as well as in the maintenance and regeneration of periodontal tissues. With regards to the fate of HERS, and although previous reports have suggested that this entails the formation of epithelial rests of Malassez, apoptosis or an epithelial-mesenchymal transformation (EMT), it is unclear what changes occur in the epithelial cells in this structure. This study examined whether HERS cells undergo EMT using a keratin-14 (K14) cre:ROSA 26 transgenic reporter mouse. The K14 transgene is expressed by many epithelial tissues, including the oral epithelium and the enamel organ. A distinct K14 expression pattern was found in the continuous HERS bi-layer and the epithelial diaphragm were visualized by detecting the ${\beta}$-galactosidase (lacZ) activity in 1 week postnatal mice. The 2 and 4 week old mice showed a fragmented HERS with cell aggregation along the root surface. However, some of the lacZ-positive dissociated cells along the root surface were not positive for pan-cytokeratin. These results suggest that the K14 transgene is a valuable marker of HERS. In addition, the current data suggest that some of the HERS cells may lose their epithelial properties after fragmentation and subsequently undergo EMT.

Cytokines Stimulate Lung Epithelial Cells to Release Nitric Oxide

  • Robbins, Richard A.;Kwon, O-Jung
    • Tuberculosis and Respiratory Diseases
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    • 제42권4호
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    • pp.447-454
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    • 1995
  • Cytokine release from alveolar macrophages and subsequent interaction of these cytokines with the bronchial epithelium can induce epithelial cells to release inflammatory mediators. Nitric oxide(NO), a highly reactive gas formed from arginine by nitric oxide synthase(NOS), is known to be involved in inflammation and edema formation, and the inducible form of NOS(iNOS) can be increased by cytokines. In this context, we hypothesized that lung epithelial cells could be stimulated by cytokines released by alveolar macrophages to express iNOS. To test this hypothesis, the murine lung epithelial cell line, LA-4, or the human lung epithelial cell line, A549, were stimulated with culture supernatant fluids from alveolar macrophages. NO production was assessed by evaluating the culture supernatant fluids for nitrite and nitrate, the stable end products of NO. Both murine and human cell culture supernatant fluids demonstrated an increase in nitrite and nitrate which were time- and dose-dependent and attenuated by $TNF{\alpha}$ and IL-$1{\beta}$ antibodies(p<0.05, all comparisons). Consistent with these observations, cytomix a combination of $TNF{\alpha}$, IL-$1{\beta}$, and $\gamma$-interferon, stimulated the lung epithelial cell lines as well as primary cultures of human bronchial epithelial cells to increase their NO production as evidenced by an increase in nitrite and nitrate in their culture supernatant fluids, an increase in the iNOS staining by immunocytochemistry, and an increase in iNOS mRNA by Northern blottin(p<0.05, all comparisons). The cytokine effects on iNOS were all attenuated by dexamethasone. To determine if these in vitro observations are reflected in vivo, exhaled NO was measured and found to be increased in asthmatics not receiving corticosteroids. These data demonstrate that alveolar macrophage derived cytokines increase iNOS expression in lung epithelial cells and that these in vitro observations are mirrored by increased exhaled NO levels in asthmatics. Increased NO in the lung may contribute to edema formation and airway narrowing.

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Cytokine Inductions and Intracellular Signal Profiles by Stimulation of dsRNA and SEB in the Macrophages and Epithelial Cells

  • Jun-Pyo Choi;Purevsuren Losol;Ghazal Ayoub;Mihong Ji;Sae-Hoon Kim;Sang-Heon Cho;Yoon-Seok Chang
    • IMMUNE NETWORK
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    • 제22권2호
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    • pp.15.1-15.16
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    • 2022
  • Foreign molecules, including viruses and bacteria-derived toxins, can also induce airway inflammation. However, to the best of our knowledge, the roles of these molecules in the development of airway inflammation have not been fully elucidated. Herein, we investigated the precise role and synergistic effect of virus-mimicking double-stranded RNA (dsRNA) and staphylococcal enterotoxin B (SEB) in macrophages and epithelial cells. To identify cytokine expression profiles, both the THP-1-derived macrophages and BEAS-2B epithelial cells were stimulated with dsRNA or SEB. A total of 21 cytokines were evaluated in the culture supernatants. We observed that stimulation with dsRNA induced cytokine production in both cell types. However, cytokine production was not induced in SEB-stimulated epithelial cells, compared to the macrophages. The synergistic effect of dsRNA and SEB was evaluated observing cytokine level and intracellular phospho-signaling. Fifteen different types were detected in high-dose dsRNA-stimulated epithelial cells, and 12 distinct types were detected in macrophages; those found in macrophages lacked interferon production compared to the epithelial cells. Notably, a synergistic effect of cytokine induction by co-stimulation of dsRNA and SEB was observed mainly in epithelial cells, via activation of most intracellular phosphor-signaling. However, macrophages only showed an accumulative effect. This study showed that the type and severity of cytokine productions from the epithelium or macrophages could be affected by different intensities and a combination of dsRNA and SEB. Further studies with this approach may improve our understanding of the development and exacerbation of airway inflammation and asthma.

흉선종의 세포학적 검색 (Cytologic Study of Thymoma)

  • 공구;장세진;이중달
    • 대한세포병리학회지
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    • 제1권1호
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    • pp.36-42
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    • 1990
  • The fluoroscopy-guided fine needle aspiration biopsy has been gaining widespread acceptance as a rapid and effective method to make a pre-operative diagnosis of mediastinal tumors including thymoma, malignant lymphoma, and metastatic carcinoma. Although thymoma is a most common tumor of the superior mediastinum, most cytopathologists are not experted in cytologic diagnosis of this tumor because of limited experience. In order to define the diagnostic cytologic features of thymoma, we have retrospectively reviewed imprinting smears and corresponding tissue sections from four cases of this tumor. All cases revealed an apparent biphasic pattern of epithelial cell clusters and lymphocytes with occasional branching capillary fronds extending from three dimensional epithelial cell clusters. Epithelial cell clusters predominated in one case and lymphocytes in two cases. Mixed epithelial cell and lymphocyte type represented in one of four cases. In the lymphocyte predominant type, the presence of epithelial cell clusters and small mature lymphocytes are helpful features to differentiate from a malignant lymphoma.

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Epithelial-Mesenchymal Interactions for the Development of Intestinal Villi

  • Oh, Seunghoon;Yoo, Young Bok
    • 한국발생생물학회지:발생과생식
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    • 제23권4호
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    • pp.305-311
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    • 2019
  • Small intestine has a structure called villi that increases the mucosal surface area for nutrient absorption. Intricate and tight epithelial-mesenchymal interactions are required for villi development. These interactions are regulated by signaling molecules, physical forces, and epithelial deformation. Signaling molecules include hedgehog (Hh), bone morphogenetic protein (BMP) and Wnt ligands. The Hh ligand is expressed from the epithelium and binds to the underlying mesenchymal cells, resulting in aggregation into mesenchymal clusters. The clusters express BMP and Wnt ligands to control its size and spacing between clusters. The clusters then form villi. Despite the fact that the villi formation is studied extensively, we do not have a complete understanding. In addition, the recent study shows there is a great relationship between the overexpression of the Hh signal and development of cancer in the gastrointestinal tract. Therefore, signaling between epithelial and mesenchymal cells and their physical interactions will be discussed on this review.

인체상피세포를 이용한 Vinyl acetate의 발암성 및 작용기전 (HIGH DOSE EXPOSURES OF VINYL ACETATE INDUCE NEOPLASTIC TRANSFORMATION OF HUMAN EPITHELIAL CELLS IN CULTURE)

  • 조준현;김진수
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제33권5호
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    • pp.437-444
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    • 2007
  • Vinyl acetate has been widely used for the manufacture of polyvinyl alcohol emulsion, which is primary ingredient of adhesive, paints, textile, paperboard coatings, etc. Since these products are plentiful and frequently used around us, workers and consumers are at health risk. International Agency for Research on Cancer(IARC) classified vinyl acetate as group 2B(possibly carcinogenic to humans). Among the organs targeted, the oral cavity is the most vulnerable organ affected by the carcinogenic effects of vinyl acetate. Since the origin of most of oral cancer is derived from the epithelial cells, it is important to understand the carcinogenic potential of vinyl acetate in human epithelial cells. Thus, the present study has attempted to utilize the immortalized human epithelial cell model to assess the carcinogenic potency of this chemical and to understand the underlying mechanisms.

기관(氣管) 상피세포 생리 및 약리 실험모델로서의 공기-액체 접면 일차배양법 연구 (Studies on the Air-Liquid Interface Culture as an Experimental Model for Physiology and Pharmacology of Tracheal Epithelial Cells)

  • 이충재;이재흔;석정호;허강민
    • Biomolecules & Therapeutics
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    • 제10권4호
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    • pp.281-286
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    • 2002
  • In this study, we intended to get a preliminary data for establishing rat tracheal surface epithelial(RTSE) cell culture system as an experimental model for physiology and pharmacology of tracheal epithelial cells. Primary culture on the membrane support and application of the air-liquid interface system at the level of cell layer were performed. The cell growth rate and mucin production rate were measured according to the days in culture. The results were as follows: this culture system was found to manifest mucocilliary differentiation of rat tracheal epithelial cells, the cells were confluent and the quantity of produced and released mucin was highest on culture day 9, the mucin was mainly released to the apical side and tbe free $^3{H}$-glucosamine which was not incorporated to process of synthesis of mucin was left on the basolateral side. Taken together, we suggest that air-liquid interface culture system can be used as a substitute for immersion culture system and as an experimental model for in vivo mucus-hypersecretory diseases.

Cell Lineage, Self-Renewal, and Epithelial-to-Mesenchymal Transition during Secondary Neurulation

  • Kawachi, Teruaki;Tadokoro, Ryosuke;Takahashi, Yoshiko
    • Journal of Korean Neurosurgical Society
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    • 제64권3호
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    • pp.367-373
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    • 2021
  • Secondary neurulation (SN) is a critical process to form the neural tube in the posterior region of the body including the tail. SN is distinct from the anteriorly occurring primary neurulation (PN); whereas the PN proceeds by folding an epithelial neural plate, SN precursors arise from a specified epiblast by epithelial-to-mesenchymal transition (EMT), and undergo self-renewal in the tail bud. They finally differentiate into the neural tube through mesenchymal-to-epithelial transition (MET). We here overview recent progresses in the studies of SN with a particular focus on the regulation of cell lineage, self-renewal, and EMT/MET. Cellular mechanisms underlying SN help to understand the functional diversity of the tail in vertebrates.

AMPK-induced mitochondrial biogenesis decelerates retinal pigment epithelial cell degeneration under nutrient starvation

  • Yujin Park;Yeeun Jeong;Sumin Son;Dong-Eun Kim
    • BMB Reports
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    • 제56권2호
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    • pp.84-89
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    • 2023
  • The implications of nutrient starvation due to aging on the degeneration of the retinal pigment epithelium (RPE) is yet to be fully explored. We examined the involvement of AMPK activation in mitochondrial homeostasis and its relationship with the maintenance of a healthy mitochondrial population and epithelial characteristics of RPE cells under nutrient starvation. Nutrient starvation induced mitochondrial senescence, which led to the accumulation of reactive oxygen species (ROS) in RPE cells. As nutrient starvation persisted, RPE cells underwent pathological epithelial-mesenchymal transition (EMT) via the upregulation of TWIST1, a transcription regulator which is activated by ROS-induced NF-κB signaling. Enhanced activation of AMPK with metformin decelerated mitochondrial senescence and EMT progression through mitochondrial biogenesis, primed by activation of PGC1-α. Thus, by facilitating mitochondrial biogenesis, AMPK protects RPE cells from the loss of epithelial integrity due to the accumulation of ROS in senescent mitochondria under nutrient starvation.

The Signaling Mechanism of TGF-β1 Induced Bovine Mammary Epithelial Cell Apoptosis

  • Di, He-Shuang;Wang, Li-Gang;Wang, Gen-Lin;Zhou, Lei;Yang, Yuan-Yuan
    • Asian-Australasian Journal of Animal Sciences
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    • 제25권3호
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    • pp.304-310
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    • 2012
  • The present study showed that Transforming growth factor beta 1 (TGF-${\beta}_1$) can induce apoptosis of bovine mammary epithelial cells. This apoptosis was also observed with phosphorylation of Smad2/3 within 0.5-2 h. Afterwards the signal transferred into the nucleus. Moreover, intracellular free $Ca^{2+}$ concentration was significantly elevated as well as Caspase-3 activated and DNA lysised, thereby inducing the programmed cell death. This signaling pathway of TGF-${\beta}_1$ was blocked by SB-431542 ($10^{-2}{\mu}M$) via inhibiting ALK-5 kinase activity, which thus reversed the anti-proliferation and apoptosis effect of TGF-${\beta}_1$ in mammary epithelial cells. These results indicated that TGF-${\beta}_1$ induced apoptosis of bovine mammary epithelial cells through the ALK-5-Smad2/3 pathway, which plays an important role in inhibiting survival of mammary epithelial cells. Moreover, intracellular $Ca^{2+}$ also played a critical role in TGF-${\beta}_1$-induced cell apoptosis.