Browsing by Subject "EPITHELIAL-CELLS"

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    The glycosylation status of murin postnatal thymus
    (SPRINGER) Balcan, E; Gümüs, A; Sahin, M
    During the intrathymic development, the fate of the thymocytes depends largely on variable expression of CD4/CD8 markers and T cell receptor protein expressions. In addition, changes of cell surface glycosylation status also affect the thymocyte maturation. In this study the glycosylation alterations in thymic tissues from 1, 9, 13 and 16 days old mice were evaluated by histochemical and lectin blotting techniques. With alcian blue (AB) at pH 5.7/periodic acid-Schiff (PAS) stainings, it was shown that thymic microenvironments contained carboxlylated and sulfated glycosaminoglycans (GAGs). Strong positivity to AB at pH 2.5, which specific for sialomucins, was seen in some medullary thymocytes. Similarly, it was shown that with Maackia amurensis agglutinin (MAL) medullary thymocytes, but not cortical ones, contained alpha(2 -> 3) linked sialic acid structures. On the other hand, while reaction with peanut agglutinin (PNA), which specific for core disaccharide galactose beta(1 -> 3) N-acetylgalactosamine, was only seen in cortical thymocytes, reaction with Galanthus nivalis agglutinin (GNA), which specific for terminal mannose residues, was seen in both cortex and medulla. However, Datura stramonium agglutinin (DSA), which recognizes galactose beta(1 -> 4) N-acetylglucosamine, was not only cell-specific, but it was bound some thymic vessels. With lectin blotting studies, five glycoprotein bands of molecular weights similar to 39, similar to 54, 100, similar to 110 and similar to 212 were found which reacted with MAL, PNA and DSA as well as GNA. These results suggest that glycosylation patterns of cell surface glycoconjugates are modified during thymocyte selection processes of postnatal days.
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    Gingival crevicular fluid interleukin-36β (-1F8), interleukin-36γ (-1F9) and interleukin-33 (-1F11) levels in different periodontal disease
    (PERGAMON-ELSEVIER SCIENCE LTD) Kursunlu, SF; Öztürk, VÖ; Han, B; Atmaca, H; Emingil, G
    Background: Periodontal inflammation is driven by the coordinated action of a number of factors, including the IL-1 family. Our study aimed to examine the levels of interleuldn (IL)-36 beta, IL-36 gamma and IL-33 levels in gingival crevicular fluid (GCF) from patients with different periodontal diseases. Materials and methods: A total of 80 subjects, 20 patients with generalized aggressive periodontitis (G-AgP), 20 patients with chronic periodontitis (CP), 20 with gingivitis and 20 periodontally healthy subjects were included. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, papillary bleeding index and plaque index. GCF cytokine levels were analysed by ELISA. Results: CP, gingivitis and healthy groups had similar GCF IL-36 beta total amount (p > 0.008). G-AgP group had elevated IL-36 beta total amount compared to CP group (p < 0.008). G-AgP group had similar GCF IL-36 beta total amount to gingivitis and healthy groups (p > 0.008). GCF IL-36 gamma and IL-33 total amounts of the study groups were similar (p > 0.05). Conclusions: The present study demonstrated for the first time the presence of IL-36 beta, IL-36 gamma and IL-33 GCF levels with different periodontal diseases. High levels of IL-36-beta in the AgP group in comparison to CP group might suggest that periodontitis in the aggressive form could be related to the increase in GCF IL-36 beta. (C) 2014 Elsevier Ltd. All rights reserved.
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    Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions
    (PERGAMON-ELSEVIER SCIENCE LTD) Tepedelen, BE; Soya, E; Korkmaz, M
    Aims: Benign prostatic hyperplasia (BPH) is the most common urological disease that is characterized by the excessive growth of prostatic epithelial and stromal cells. Pharmacological therapy for BPH has limited use due to the many side effects so there is a need for new agents including natural compounds such as epigallocatechin-3-gallate (EGCG). This study was undertaken to assess the role of EGCG, suppressing the formation of BPH by reducing inflammation and oxidative stress, in cytoskeleton organization and ECM interactions via focal adhesions. Main methods: We performed MTT assay to investigate cell viability of BPH-1 cells, wound healing assay to examine cell migration, immunofluorescence assay for F-actin organization and paxillin distribution and finally immunoblotting to investigate focal adhesion protein levels in the presence and absence of EGCG. Key findings: We found that EGCG inhibits cell proliferation at the concentration of 89.12 mu M, 21.2 mu M and 2.39 mu M for 24, 48 and 72 h, respectively as well as inhibitory effects of EGCG on BPH-1 cell migration were observed in a wound healing assay. Furthermore, it was determined by immunofluorescence labeling that EGCG disrupts F-actin organization and reduces paxillin distribution. Additionally, EGCG decreases the activation of FAK (Focal Adhesion Kinase) and the levels of paxillin, RhoA (Ras homolog gene family, member A), Cdc42 (cell division cycle 42) and PAK1 (p21 protein-activated kinase 1) in a dose-dependent manner. Significance: For the first time, by this study, we found evidence that BPH-1 cell proliferation could be inhibited with EGCG through the disruption of cytoskeleton organization and ECM interactions. Consequently, EGCG might be useful in the prevention and treatment of diseases characterized by excessive cell proliferation such as BPH.