Estudo da função do receptor de peptídeos formilados 2 (FPR2) no tabagismo: foco na transição epitelial mesenquimal

Abstract

In the airways, the epithelial-mesenchymal transition (EMT) has been implicated in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). Aspirin-triggered resolvin D1 (AT-RvD1) is known to be involved in the resolution of inflammation and inhibits TGF β1-induced EMT on A549 cells. Here, we extend this results and evaluated the role of AT RvD1 in EMT induced by cigarette smoke extract (CSE) on bronchial epithelial cells (BEAS 2B). CSE increased TGF-β1 production and the mesenquimal markers (N-cadherin, vimentin, SMAD2/3 and Slug) expressions. In addition, CSE decreased E-cadherin expression, an epithelial marker. Furthermore, CSE induced an increase in ROS and FPR2 receptor expression. When AT-RvD1 was associated, there was restored the expression of E-cadherin and reduced expression of N-cadherin, vimentin and SMAD2/3 and TGF-β1 production on BEAS-2B cells stimulated by CSE. In addition, AT-RvD1 decreased ROS and FPR2 levels. In conclusion, our results demonstrate that AT-RvD1 decreased CSE-induced EMT by restored the expression of E-cadhrein and inhibit the TGF-β1 and ROS production and expression of N-cadherin, vimentin and SMAD2/3. Together, these results suggest that AT RvD1 has the potential to control epithelial-mesenchymal transition.