Alterations at the Synthesis and Degradation of E-cadherin in the Human Lungs with Emphysema

Year 2017, Volume: 76 Issue: 2, 61 - 68, 27.12.2017

Ecem Gogus Ozgecan Kayalar H. Gul Ongen Fusun Oztay

https://doi.org/10.5152/EurJBiol.2017.1711

Abstract

Pulmonary emphysema leads to a cascade of
events starting with enlarged alveoli, loss of alveoli and, subsequently to the
damage and disruption of pulmonary epithelium. The integrity of the pulmonary
epithelium, which is constituted by pneumocytes linked to each other through
E-cadherin proteins, is important for respiration. The aim of the present study
was to detect the content and destruction of E-cadherin protein and to
investigate the contribution of E-cadherin to pulmonary emphysema pathogenesis.

The structural changes, reparative capacity
of the pulmonary epithelium, amount of E-cadherin protein and, the
immunoreactivity of neural precursor cell expressed developmentally
down-regulated protein 9 (NEDD9) were evaluated in emphysematous (n=7) and
non-emphysematous (n=6) areas of lung samples taken from patients with chronic
obstructive pulmonary disease. Emphysematous areas are characterized by
enlarged alveoli, disrupted alveolar walls and epithelium, increased type 2
pneumocytes and NEDD9 immunoreactivity, and reduced E-cadherin proteins.

Our
data shows that E-cadherin levels are decreased in emphysematous areas due to
its degradation by NEDD9. Decreased E-cadherin levels also lead to the
disintegration of the pulmonary epithelium by causing the presence of weakness
intercellular connections or the absence of intercellular connections. The
repair of the pulmonary epithelium could not complete due to the reduced
E-cadherin, because type 2 pneumocytes could not differentiate into type 1
pneumocytes. In conclusion, the reduced E-cadherin levels lead to emphysematous
alterations in human lungs and contributes to pulmonary emphysema pathogenesis.

Keywords

Pulmonary emphysema, COPD, E-cadherin, pulmonary epithelium

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