• The korean journal of orthodontics
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• v.31 no.1 s.84
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• pp.71-83
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• 2001

The purpose of this study was to Prove that the medial edge epithelial cells covering the secondary palatal shelves were removed by apoptosis during palatal fusion. 12 mature female rats (Suprague-Dawley) were mated overnight with male rats and sacrificed on days 15.0, 16.5, 16.75, 17.0 of pregnancy. The embryos were removed from the uterus and the heads were embedded in paraffin. The paraffin blocks were sectioned and the sections were undergone H-E staining for general histologic feature and TdT staining for detection of apoptotic cells. The obtained results were as follows. k. In the section of 16.0 and 16.5 day embryos, the palatal shelves were prior to contact and no apoptotic cells wereobserved in the medial edge epithelium. At the initial contact of Palatal shelves, there was a few apoptotic cells in the fusing epithelium. 2. In the 16.75 day embryos, the samples that epithelial seams did not lost there continuity, apoptotic cells were rarely seen at the midline epithelial seam. In contrast, a lot of apoptotic cells were observed at epithelial triangles and the junction between palatal shelves and nasal septum. 3. In the 16,75 day embryos, the samples that epithelial seams lost their continuity and disrupted to epithelial islands, large number, of apoptotic cells were observed at epithelial islands and epithelial triangles. Some apoptotic cells were also observed at the oral, nasal epithelium near the midline. 4. In the 17.0 day embryos, most of epithelial islands were disappeared and mesenchymal confluence was achieved. Apoptotic cells were rarely observed in the mesenchymal tissue which replaced epithelial islands, but there were some apoptotic cells at the epithelial triangles, oral and nasal epithelium. From the results of the study, it was revealed that medial edge epithelial cells of fusing palate were removed by apoptosis. Apoptotic cells were found mainly in the disappearing midline epithelial seam and the oral and nasal epithelial triangles at some late stages of palatal fusion.

• Journal of Life Science
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• v.10 no.1
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• pp.37-44
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• 2000

The mammary gland contains a subpopulation of epithelial cells with large proliferative potentials which are the likely targets for carcinogens. These clonogenic cells can proliferate and differentiate into functional glandular structures. Rat mammary epithelial cells (RMEC) were isolated and characterized in vitro. By flow cytometry of RMEC stained with fluorescein isothiocyanate-peanut agglutinin(PNA) and phycoerythrin anti-Thy-1.1 monoclonal antibody, it was possible to four cell subpopulations from 7-8 week old F344 female rat mammary glands: cells negative to both reagents (B-), PNA-positive cells (PNA+), Thy-1.1-positive cells (Thy-1.1+), and cells positive to both reagents (B+). When single PNA+ cells were isolated and cultured in Matrigel with irradiated (∼50 Gray) 3T3 fibroblast feeder layer, they gave rise to multicellular clonal structures of three types: alveolar, foamy alveolar, and squamous colonies. The developed structures were similar to the mammary glands in vivo. These results suggest that some of PNA+ cells possesses many of the characteristics of multipotent clonogenic stem-like cells.

• Natural Product Sciences
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• v.15 no.4
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• pp.185-191
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• 2009

Intestinal epithelial cells (IEC) play an important role in the mucosal immune system. IEC-derived mediators of inflammatory cascades play a principal role in the development of colon inflammation. The aim of this study was to investigate the inhibitory effect of aqueous extracts of Schizandra chinensis fruits (SC-Ex) on the production of inflammatory mediators by the human colonic epithelial cells. HT-29 cells were stimulated with dextran sulfate sodium in the presence or absence of SC-Ex to examine the cytoprotection and production of IL-8 and reactive oxygen species (ROS). It was shown that dextran sulfate sodium (DSS) caused the reduction of cell viability and production of IL-8 and ROS in DSS-treated HT-29 cells. We observed that the treatment of SC-Ex protected significantly cell proliferation from DSS-induced damage in dose-dependent manner. SC-Ex (10 and 100 ${\mu}g$/ml) also suppressed DSS-induced production of IL-8 mRNA and protein. Moreover, DSS-induced ROS production was inhibited markedly by the treatment of 100 ${\mu}g$/ml SC-Ex. These results suggest that SC-Ex has the protective effects on DSS-induced cell damage and the release of inflammatory mediators in the intestinal epithelial cells.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.117-122
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• 2015

BACKGROUND/OBJECTIVES: Curcumin, a major component of the Curcuma species, contains antioxidant and anti-inflammatory properties. Although it was found to induce apoptosis in cancer cells, the functional role of curcumin as well as its molecular mechanism in anti-inflammatory response, particularly in intestinal cells, has been less investigated. The intestine epithelial barrier is the first barrier and the most important location for the substrate coming from the lumen of the gut. SUBJECTS/METHODS: We administered curcumin treatment in the human intestinal epithelial cell lines, T84 and Caco-2. We examined endoplasmic reticulum (ER) stress response by thapsigargin, qPCR of XBP1 and BiP, electrophysiology by wild-type cholera toxin in the cells. RESULTS: In this study, we showed that curcumin treatment reduces ER stress and thereby decreases inflammatory response in human intestinal epithelial cells. In addition, curcumin confers protection without damaging the membrane tight junction or actin skeleton change in intestine epithelial cells. Therefore, curcumin treatment protects the gut from bacterial invasion via reduction of ER stress and anti-inflammatory response in intestinal epithelial cells. CONCLUSIONS: Taken together, our data demonstrate the important role of curcumin in protecting the intestine by modulating ER stress and inflammatory response post intoxication.

• Biotechnology and Bioprocess Engineering:BBE
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• v.3 no.1
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• pp.1-5
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• 1998

One cervical cancer cell line, C9, carrying human papillomavirus type 18 (HPV18) genes that is one of the major etiologic concoviruses for cervical cancer was characterized. This cell line was further characterized for its capacity related to the epithelial cell proliferation, stratification and differentiation in reconstituted artificial epithelial tissue. The in vitro construction of three dimensional artificial cervical opithelial tissue has been engineered using C9 epithelial cancer cells, human foreskin fibroblasts and a matrix made of type I collagen by organotypic culture of epithelial cells. The morphology of paraffin embedded artificial tissue was examined by histochemical staining. The artificial epithelial tissues were well developed having multilayer. However, the tissue morphology was similar to the cervical tissus having displasia induced by HPV infection. The characteristics of the artificial tissues were examined by determinining the expression of specific marker proteins. In the C9 derived artificial tissues, the expression of EGF receptor, as epithelial proliferation marker proteins for stratum basale was observed up to the stratum spinosum. Another epithelial proliferation marker for stratum spinosum, cytokerations 5/6/18, were observed well over the stratum spinosum. For the differentiation markers, the expression of involucrin and filaggrin were observed while the terminal differentiation marker, cytokeratins 10/13 was not detected at all. Therefore the reconstituted artificial epithelial tissues expressed the same types of differentiation marker proteins that are expressed in normal human cervical epithelial tissues but lacked the final differentiation capacity representing characteristics of C9 cell line as a cancer tissue devived cell line. Expression of HPV18 E6 oncoprotein was also observed in this artifical cervical opithelial tissue though the intensity of the staining was weak. Thus this artificial epithelial tissue could be used as a useful model system to examine the relationship between HPV-induced cervical oncogenesis and epithelial cell differentiation.

• Asian-Australasian Journal of Animal Sciences
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• v.15 no.8
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• pp.1198-1203
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• 2002

To understand molecular mechanisms involved in bovine mammary gland growth, expression of stat5a gene was examined in bovine mammary tissues. We found that stat5a gene was highly induced at pregnant 7 and 8 months compared to virgin mammary tissues. To examine function of bovine stat5a in mammary epithelial cell proliferation, stat5a expression vector was transfected into mammary epithelial HC11 cells. Cell proliferation rate in stat5a gene-transfected cells was 26%, 95% and 85% higher at 24 h, 48 h and 72 h after seeding, respectively, compared to control vector-transfected cells. Results demonstrate that bovine stat5a enhances proliferation of mammary epithelial cells.

• Biomolecules & Therapeutics
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• v.30 no.2
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• pp.170-178
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• 2022

The airway epithelium is equipped with the ability to resist respiratory disease development and airway damage, including the migration of airway epithelial cells and the activation of TLR3, which recognizes double-stranded (ds) RNA. Primary cilia on airway epithelial cells are involved in the cell cycle and cell differentiation and repair. In this study, we used Beas-2B human bronchial epithelial cells to investigate the effects of the TLR3 agonist polyinosinic:polycytidylic acid [Poly(I:C)] on airway cell migration and primary cilia (PC) formation. PC formation increased in cells incubated under serum deprivation. Migration was faster in Beas-2B cells pretreated with Poly(I:C) than in control cells, as judged by a wound healing assay, single-cell path tracking, and a Transwell migration assay. No changes in cell migration were observed when the cells were incubated in conditioned medium from Poly(I:C)-treated cells. PC formation was enhanced by Poly(I:C) treatment, but was reduced when the cells were exposed to the ciliogenesis inhibitor ciliobrevin A (CilioA). The inhibition of Beas-2B cell migration by CilioA was also assessed and a slight decrease in ciliogenesis was detected in SARS-CoV-2 spike protein (SP)-treated Beas-2B cells overexpressing ACE2 compared to control cells. Cell migration was decreased by SP but restored by Poly(I:C) treatment. Taken together, our results demonstrate that impaired migration by SP-treated cells can be attenuated by Poly(I:C) treatment, thus increasing airway cell migration through the regulation of ciliogenesis.

• Applied Microscopy
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• v.21 no.1
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• pp.46-62
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• 1991

The intermediate filament is one of the most important constituents of the intracytoplasmic cytoskeleton microtubule, actin, myosin and intermediate filament. It is composed of keratin, desmin, vimentin, neurofilament and glial filament, and has important role as a cellular marker, epithelial or mesenchymal origin. So it will be important to differentiated from some poorly or undifferentiated neoplasm to provide adequate therapeutic modalities. This study was performed by using immunohistochemical staining and electron microscopic observation to find out intermediate filaments of epithelial and non-epithelial tumor cells evaluate the degree of differentiation in tumors and therefore to provide some diagnostic and therapeutic modalities. The materials consisted of 83 epithelial and non-epithelial elements bearing 23 normal control, 28 epithelial tumors, and 32 non-epithelial tumors, that are resected for definite treatment at Chosun University Hospital from June, 1988 to June, 1990. Immunohistochemical stain for keratin, desmin and vimentin, and electron microscopic study were performed in all cases. The results obtained were as follows. 1. Immunohistochemical stain for intermediate filament were very useful diagnostic aid for differentiated epithelial tumor to non-epithelial tumor in diagnostic neoplasia. 2. In the electron microscopic finding, the size of intermediate filaments were possible differentiated to cell components of epithelial tumor and non-epithelial tumors.

• International Journal of Oral Biology
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• v.36 no.3
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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.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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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.