Comment on: Transcriptomic analysis of CFTR-impaired endothelial cells reveals a pro-inflammatory phenotype

We read with interest the article "Transcriptomic analysis of CFTR-impaired endothelial cells reveals a pro-inflammatory phenotype" by Declercq et al. [1]. Cystic fibrosis transmembrane conductance regulator (CFTR) is a cyclic adenosine monophosphate (cAMP)-dependent and ATP-gated Cl– channel and mutations in the CFTR gene are responsible for cystic fibrosis (CF) [2]. Declercq et al. [1] report that CFTR impairment in endothelial cells (ECs) by CFTR silencing or inhibition (using CFTR inhibitor 172, CFTRinh-172) reduced EC proliferation, migration and autophagy. Moreover, the authors demonstrated that the loss of CFTR acts in favour of EC dysfunction characterised by pro-inflammatory phenotype favouring leukocyte extravasation. Using cftr knock-out (KO) mice, Declercq et al. [1] found an increase of leukocyte extravasation in lung and liver parenchyma associated with increased levels of EC activation markers (figure 1).
Source: European Respiratory Journal - Category: Respiratory Medicine Authors: Tags: Original Articles: Correspondence Source Type: research