Browsing by Subject "N-cadherin"

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    Myocardial Connexin-43 and N-Cadherin decrease during vanadium inhalation
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Fortoul, Teresa I.; Soto-Mota, Adrian; Rojas-Lemus, Marcela; Rodriguez-Lara, Vilaney; GonzalezVillalva, Adriana; Montaño, Luis F.; Paez, Araceli; Colin-Barenque, Laura; López-Valdez, Nelly; Cano Gutiérrez, Gumaro; Bizarro-Nevares, Patricia; Ustarroz-Cano, Martha
    Particulate matter air pollution has considerably increased during the last decades; vanadium is a transition element adhered to this particulate matter, and the combustion of fossil fuels is the main source in the atmosphere. It has been reported that air pollution and specifically vanadium exposure increases the probability of suffering arrhythmias; however the biological mechanism of such a relationship remains unknown. It has been established that a diminished presence of NCadherin alters the Connexin-43 arrangement, and the consequent altered presence of these proteins predisposes to ventricular heart rate problems. We analyzed myocardial histology and the expression of N-Cadherin and Connexin-43 by immunohistochemistry in mouse that inhaled vanadium. Our results showed a significant and progressive reduction in both N-Cadherin and Connexin-43, as well as the presence of meganucleus; myofibrils disruption, and clumping in the exposed groups were also observed. Our findings add more information about a possible explanation for the arrythmogenic effect observed in dwellers of cities with high particulate matter atmospheric pollution.
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    N-Cadherin, ADAM-10 and Aquaporin 1 expression in lung tissue exposed to fluoroedenite fibers: an immunohistochemical study
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Musumeci, Giuseppe; Loreto, Carla; Szychlinska, Marta Anna; Imbesi, Rosa; Rapisarda, Venerando; Aiello, Flavia Concetta; Castorina, Sergio; Castrogiovanni, Paola
    Fluoro-edenite (FE) fibers are similar to other amphibole asbestos fibers. The scientific relevance of FE is due to its ability to lead to chronic inflammation and carcinogenesis in lung tissue shown after its inhalation. These fibers stimulate aberrant host cell proliferation and induce the release of cytokines, growth factors, reactive oxygen and nitrite species, which results in DNA damage. In previous studies, we showed that FE induces functional modifications in sheep and human lung fibroblasts and alveolar epithelial cells, where the overexpression of several molecules probably involved in pathological cellular mechanisms induced by FE exposition have been detected. However, the mechanisms of cellular and molecular toxicity and the cellular response to FE fibers are still not well known. N-cadherin, ADAM-10 and AQP1 are molecules involved in carcinogenesis and in inflammatory process. In this study we analyzed, through immunohistochemistry, their expression in the lung tissue of sheep exposed to FE. Our results showed different patterns of immunolabeling for N-cadherin, ADAM-10 and AQP1. N-cadherin and ADAM-10 were more expressed in FE exposed lung tissue, when compared with the control. On the contrary, AQP1 was more expressed in non exposed lung tissue. These results suggest that NCadherin, ADAM-10 and AQP1 are probably involved in different pathological processes induced by FE fiber exposition. The aim of the study was to better understand the mechanisms of cellular and molecular toxicity and of cellular response to FE fibers in order to identify, in the future, a possible therapeutic intervention in cases of FE-associated pathogenesis.
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    N-cadherin, beta-catenin and connexin 43 expression in astrocytic tumours of various grades
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Reszec, J.; Szkudlarek, M.; Hermanowicz, A.; Bernaczyk, P.S.; Mariak, Z.; Chyczewsk, L.
    Introduction: Astrocytic tumors are the most common primary brain tumors, but little is known about their etiology and prognostic factors. N-cadherin and beta-catenin are adhesive proteins, and are often overexpressed in many types of cancers, including breast or colorectal cancer, resulting in better prognosis. Connexin 43 is a gap junction protein involved in cellcell signaling pathway taking part in the process of carcinogenesis. The aim of the study was to evaluate Ncadherin, beta-catenin and connexin 43 expression in astrocytic tumors of various grades. Materials and methods: We examined 131 cases of astrocytic tumors, including 26 cases of diffuse astrocytoma (group I), 44 anaplasic astrocytomas (group II) and 61 glioblastoma cases (group III) - primary and secondary. To evaluate N-cadherin, beta-catenin and connexin 43 expression, we used immunohistochemical reaction with specific antibodies (Santa Cruz Biotechnology). The obtained results were correlated with clinical and morphological features. Results: Beta-catenin expression was observed in 69.3% of diffuse astrocytomas, 75% of anaplastic astrocytomas, and 82% of glioblastoma cases. Ncadherin expression was observed in 92.3% of diffuse astrocytomas, 90.1% of anaplastic astrocytomas, and in all glioblastoma cases. Connexin 43 was observed in 76.9% of diffuse astrocytomas, and in all cases of anaplastic astrocytomas and glioblastomas. Beta-catenin expression was significant within the nucleus of neoplastic cells in groups I and II. In group III, staining was observed only in the cellular membranes. Ncadherin and connexin 43 expression was observed only in the cells’ membranes. In glioblastomas, both primary and secondary, all protein expression was significant within the cells surrounding the necroses and blood vessels and weak or absent in the tumor’s margins. Conclusion: Our study shows that beta-catenin nuclear expression in group of diffuse astrocytomas and anaplastic astrocytomas is evidence for transcriptional function of beta-catenin in those groups. Strong Ncadherin and connexin 43 expression in those groups may be evidence for their role in tumor formation and progression. However, in glioblastomas a very important role of all examined proteins is generating intracellular connections to facilitate the escape of tumor cells from the effects of hypoxia or their accumulation around the blood vessels rather than tumor invasion into the brain parenchyma.