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Comparison of a novel potentiator of CFTR channel activity to ivacaftor in ameliorating mucostasis caused by cigarette smoke in primary human bronchial airway epithelial cells.
Tanjala, Adrian Constantin; Jiang, Jia Xin; Eckford, Paul D W; Ramjeesingh, Mohabir; Li, Canhui; Huan, Ling Jun; Langeveld, Gabrielle; Townsend, Claire; Paone, Daniel V; Busch-Petersen, Jakob; Pekhletski, Roman; Tang, LiPing; Raju, Vamsee; Rowe, Steven M; Bear, Christine E.
Afiliación
  • Tanjala AC; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Jiang JX; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Eckford PDW; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Ramjeesingh M; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Li C; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Huan LJ; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Langeveld G; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Townsend C; NCE Molecular Discovery, GSK, Cambridge, USA.
  • Paone DV; NCE Molecular Discovery, GSK, Cambridge, USA.
  • Busch-Petersen J; NCE Molecular Discovery, GSK, Cambridge, USA.
  • Pekhletski R; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada.
  • Tang L; Department of Medicine, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA.
  • Raju V; Department of Medicine, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA.
  • Rowe SM; Department of Medicine, Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA.
  • Bear CE; Program in Molecular Medicine, Research Institute, Hospital for Sick Children, Toronto, Canada. bear@sickkids.ca.
Respir Res ; 25(1): 269, 2024 Jul 10.
Article en En | MEDLINE | ID: mdl-38982492
ABSTRACT

BACKGROUND:

Cystic Fibrosis causing mutations in the gene CFTR, reduce the activity of the CFTR channel protein, and leads to mucus aggregation, airway obstruction and poor lung function. A role for CFTR in the pathogenesis of other muco-obstructive airway diseases such as Chronic Obstructive Pulmonary Disease (COPD) has been well established. The CFTR modulatory compound, Ivacaftor (VX-770), potentiates channel activity of CFTR and certain CF-causing mutations and has been shown to ameliorate mucus obstruction and improve lung function in people harbouring these CF-causing mutations. A pilot trial of Ivacaftor supported its potential efficacy for the treatment of mucus obstruction in COPD. These findings prompted the search for CFTR potentiators that are more effective in ameliorating cigarette-smoke (CS) induced mucostasis.

METHODS:

Small molecule potentiators, previously identified in CFTR binding studies, were tested for activity in augmenting CFTR channel activity using patch clamp electrophysiology in HEK-293 cells, a fluorescence-based assay of membrane potential in Calu-3 cells and in Ussing chamber studies of primary bronchial epithelial cultures. Addition of cigarette smoke extract (CSE) to the solutions bathing the apical surface of Calu-3 cells and primary bronchial airway cultures was used to model COPD. Confocal studies of the velocity of fluorescent microsphere movement on the apical surface of CSE exposed airway epithelial cultures, were used to assess the effect of potentiators on CFTR-mediated mucociliary movement.

RESULTS:

We showed that SK-POT1, like VX-770, was effective in augmenting the cyclic AMP-dependent channel activity of CFTR. SK-POT-1 enhanced CFTR channel activity in airway epithelial cells previously exposed to CSE and ameliorated mucostasis on the surface of primary airway cultures.

CONCLUSION:

Together, this evidence supports the further development of SK-POT1 as an intervention in the treatment of COPD.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Bronquios / Quinolonas / Regulador de Conductancia de Transmembrana de Fibrosis Quística / Células Epiteliales / Aminofenoles Límite: Humans Idioma: En Revista: Respir Res Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Bronquios / Quinolonas / Regulador de Conductancia de Transmembrana de Fibrosis Quística / Células Epiteliales / Aminofenoles Límite: Humans Idioma: En Revista: Respir Res Año: 2024 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido