scholarly journals Epigenetic Regulation of Gene Activity in Epithelial Cells of Nasal Mucous Membrane in Patients with Polypous Rhinosinusitis

2017 ◽  
Vol 23 (1) ◽  
Author(s):  
Ivanna Koshel
Keyword(s):  
Epithelial Cell ◽  
Mucous Membrane ◽  
Functional State ◽  
Cytogenetic Study ◽  
Nasal Epithelial Cell ◽  
Nasal Mucous Membrane ◽  
Pathogenic Variants ◽  
Quantitative Characteristics ◽  
Cell Genome

Nowadays, a wide clinico-laboratory polymorphism of “polypous rhinosinusitis” is observed. It suggests the potential role of heredity in the formation of the disease indicating the necessity of studying the role of genetic factor in the formation of various clinico-pathogenic variants of polyposis in detail.The objective of the research was to study the degree of functional abnormalities in the epithelial cell genome of the nasal mucous membrane in patients with polypous rhinosinusitis using the cytogenetic methods.Materials and methods.The article presents the results of cytogenetic study of 70 patients with various types of polypous rhinosinusitis (aspirin-intolerant and allergic). Hereditary predisposition to the disease was determined applying clinical and genealogical analysis.Results.Significant differences in the quantitative characteristics of the functional state of the nasal epithelial cell genome by the criterion of chromatization indices, the nucleolar index, the indices of the heteropyknotic X chromosome and pathologically altered nuclei were found in patients with aspirin-intolerant polypous rhinosinusitis as compared to those with allergic polypous rhinosinusitis as well as the control group.The identified changes serve as a criterion of the reduction in the activity of the transcriptional-translational processes in aspirin-intolerant polypous rhinosinusitis.Conclusions.The studied changes in the parameters of the functional state of the epithelial cell genome in the nasal mucous membrane provided an objective confirmation of hypothesis about epigenetic nature of pathology formation.

The mystery behind the nostrils – technical clues for successful nasal epithelial cell cultivation

2021 ◽  
pp. 151748
Author(s):  
Malik Aydin ◽  
Ella A. Naumova ◽  
Aliyah Bellm ◽  
Ann-Kathrin Behrendt ◽  
Federica Giachero ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Cultivation ◽  
Nasal Epithelial Cell

scholarly journals Development of a Novel ex vivo Nasal Epithelial Cell Model Supporting Colonization With Human Nasal Microbiota

2019 ◽  
Vol 9 ◽  
Author(s):  
Derald D. Charles ◽  
James R. Fisher ◽  
Sarah M. Hoskinson ◽  
Audrie A. Medina-Colorado ◽  
Yi C. Shen ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Model ◽  
Ex Vivo ◽  
Nasal Epithelial Cell ◽  
Nasal Microbiota

The role of Polycomb in stem cell genome architecture

2016 ◽  
Vol 43 ◽  
pp. 87-95 ◽  
Author(s):  
Gloria Mas ◽  
Luciano Di Croce
Keyword(s):  
Stem Cell ◽  
Genome Architecture ◽  
Cell Genome

scholarly journals Role of Glycosides as Epithelial Cell Receptors for Candida albicans

Microbiology ◽  
1987 ◽  
Vol 133 (3) ◽  
pp. 637-643 ◽  
Author(s):  
I. A. CRITCHLEY ◽  
L. J. DOUGLAS
Keyword(s):  
Candida Albicans ◽  
Epithelial Cell ◽  
Cell Receptors

scholarly journals Neuropeptide Y (NPY) promotes inflammation-induced tumorigenesis by enhancing epithelial cell proliferation

2017 ◽  
Vol 312 (2) ◽  
pp. G103-G111 ◽  
Author(s):  
Sabrina Jeppsson ◽  
Shanthi Srinivasan ◽  
Bindu Chandrasekharan
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Neuropeptide Y ◽  
Intestinal Inflammation ◽  
Enteric Neurons ◽  
Intestinal Epithelial ◽  
Epithelial Proliferation ◽  
Proliferation And Apoptosis

We have demonstrated that neuropeptide Y (NPY), abundantly produced by enteric neurons, is an important regulator of intestinal inflammation. However, the role of NPY in the progression of chronic inflammation to tumorigenesis is unknown. We investigated whether NPY could modulate epithelial cell proliferation and apoptosis, and thus regulate tumorigenesis. Repeated cycles of dextran sodium sulfate (DSS) were used to model inflammation-induced tumorigenesis in wild-type (WT) and NPY knockout ( NPY−/−) mice. Intestinal epithelial cell lines (T84) were used to assess the effects of NPY (0.1 µM) on epithelial proliferation and apoptosis in vitro. DSS-WT mice exhibited enhanced intestinal inflammation, polyp size, and polyp number (7.5 ± 0.8) compared with DSS- NPY−/− mice (4 ± 0.5, P < 0.01). Accordingly, DSS-WT mice also showed increased colonic epithelial proliferation (PCNA, Ki67) and reduced apoptosis (TUNEL) compared with DSS- NPY−/− mice. The apoptosis regulating microRNA, miR-375, was significantly downregulated in the colon of DSS-WT (2-fold, P < 0.01) compared with DSS- NPY−/−-mice. In vitro studies indicated that NPY promotes cell proliferation (increase in PCNA and β-catenin, P < 0.05) via phosphatidyl-inositol-3-kinase (PI3-K)-β-catenin signaling, suppressed miR-375 expression, and reduced apoptosis (increase in phospho-Bad). NPY-treated cells also displayed increased c-Myc and cyclin D1, and reduction in p21 ( P < 0.05). Addition of miR-375 inhibitor to cells already treated with NPY did not further enhance the effects induced by NPY alone. Our findings demonstrate a novel regulation of inflammation-induced tumorigenesis by NPY-epithelial cross talk as mediated by activation of PI3-K signaling and downregulation of miR-375. NEW & NOTEWORTHY Our work exemplifies a novel role of neuropeptide Y (NPY) in regulating inflammation-induced tumorigenesis via two modalities: first by enhanced proliferation (PI3-K/pAkt), and second by downregulation of microRNA-375 (miR-375)-dependent apoptosis in intestinal epithelial cells. Our data establish the existence of a microRNA-mediated cross talk between enteric neurons producing NPY and intestinal epithelial cells, and the potential of neuropeptide-regulated miRNAs as potential therapeutic molecules for the management of inflammation-associated tumors in the gut.

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