Publication: N-Cadherin, ADAM-10 and Aquaporin 1
expression in lung tissue exposed to fluoroedenite fibers: an immunohistochemical study
Authors
Musumeci, Giuseppe ; Loreto, Carla ; Szychlinska, Marta Anna ; Imbesi, Rosa ; Rapisarda, Venerando ; Aiello, Flavia Concetta ; Castorina, Sergio ; Castrogiovanni, Paola
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-11-603
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info:eu-repo/semantics/article
Description
Abstract
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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