FFC#23/2014

Mechanisms and clinical implications of endothelial dysfunction in cystic fibrosis

FFC#23/2014

Mechanisms and clinical implications of endothelial dysfunction in cystic fibrosis

PRINCIPAL INVESTIGATOR

Mario Romano (Dip. di Scienze Sperimentali e Cliniche, Lab. di Medicina Molecolare, Università G. D’Annunzio, Chieti-Pescara)

Partner

Licia Totani (Dip. di Farmacologia Traslazionale, Consorzio Mario Negri Sud/Unità di Biomarkers Vascolari, Chieti) Marco Marchisio (Dip. di Medicina e Scienze dell’Invecchiamento, Lab. sul Signalling Cellulare, Università G. D’Annunzio, Chieti-Pescara)

RESEARCHERS

16

CATEGORY

AREA 4 Lung inflammation

DURATION

2 years

GOAL

€ 60.000

RESULTS

Endothelial cells were isolated from pulmonary artery (CF-PAEC) of explanted CF lungs and CFTR activity was measured using patch clamping. With experiments under static condition or shear stress provocation, the study demonstrated that CF-PAEC reduced monolayer integrity and transendothelial electric resistance (TEER); further, a high number of microvescicles (EMV) was released. EMV were increased in peripheral blood of CF patients and inversely correlated with respiratory indices. In attempt to uncover molecular signatures of CFTR dysfunction in EC, they evaluated microRNA expression in CF-PAEC, identifying some microRNA overexpressed and others with low amount. Agents that increase cAMP levels such as phosphodiesterase inhibitors and beta adrenergic receptor agonists corrected TEER and monolayer integrity of CF-PAEC. These results encourage further studies on miRNA and transcellular communication pathways as well on the clinical utility of cAMP increasing drugs to correct the endothelial dysfunction in CF.

OTHER RESULTS

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Some peptide nucleic acids (PNAs) re-sensitise Pseudomonas aeruginosa to the antibiotic meropenem in vitro and reduce its virulence.

FFC#1/2023

Tezacaftor, one of the components of Kaftrio, induces an accumulation of dihydroceramides both in vitro and in vivo in animal models