Extent of rescue of F508del-CFTR function by VX-809 and VX-770 in human nasal epithelial cells correlates with SNP rs7512462 in SLC26A9 gene in F508del/F508del Cystic Fibrosis patients

Biochim Biophys Acta Mol Basis Dis. 2019 Jun 1;1865(6):1323-1331. doi: 10.1016/j.bbadis.2019.01.029. Epub 2019 Feb 1.

Abstract

Background: We analyzed the CFTR response to VX-809/VX-770 drugs in conditionally reprogrammed cells (CRC) of human nasal epithelium (HNE) from F508del/F508del patients based on SNP rs7512462 in the Solute Carrier Family 26, Member 9 (SLC26A9; MIM: 608481) gene.

Methods: The Isc-eq measurements of primary nasal epithelial cells from F508del/F508del patients (n = 12) for CFTR function were performed in micro Ussing chambers and compared with non-CF controls (n = 2). Data were analyzed according to the rs7512462 genotype which were determined by real-time PCR.

Results: The CRC-HNE cells from F508del/F508del patients evidenced high variability in the basal levels of CFTR function. Also, the rs7512462*C allele showed an increased basal CFTR function and higher responses to VX-809 + VX-770. The rs7512462*CC + CT genotypes together evidenced CFTR function levels of 14.89% relatively to wt/wt (rs7512462*CT alone-15.29%) i.e., almost double of rs7512462*TT (7.13%). Furthermore, sweat [Cl-] and body mass index of patients also evidenced an association with the rs7512462 genotype.

Conclusion: The CFTR function can be performed in F508del/F508del patient-derived CRC-HNEs and its function and responses to VX-809 + VX-770 combination as well as clinical data, are all associated with the rs7512462 variant, which partially sheds light on the generally inter-individual phenotypic variability and in personalized responses to CFTR modulator drugs.

Keywords: CFTR; CFTR modulator drugs; CRC-HNE; Cystic fibrosis; Modifier genes; SLC26A9; Ussing chamber.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Aminophenols / pharmacology*
  • Aminopyridines / pharmacology*
  • Antiporters / genetics*
  • Antiporters / metabolism
  • Base Sequence
  • Benzodioxoles / pharmacology*
  • Body Mass Index
  • Case-Control Studies
  • Cellular Reprogramming
  • Chloride Channel Agonists / pharmacology*
  • Cystic Fibrosis / genetics
  • Cystic Fibrosis / metabolism
  • Cystic Fibrosis / pathology
  • Cystic Fibrosis Transmembrane Conductance Regulator / deficiency
  • Cystic Fibrosis Transmembrane Conductance Regulator / genetics*
  • Diffusion Chambers, Culture
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Epithelial Cells / pathology
  • Gene Expression
  • Genotype
  • Humans
  • Models, Biological
  • Nasal Mucosa / drug effects
  • Nasal Mucosa / metabolism
  • Nasal Mucosa / pathology
  • Polymorphism, Single Nucleotide
  • Primary Cell Culture
  • Quinolones / pharmacology*
  • Sequence Deletion
  • Sulfate Transporters / genetics*
  • Sulfate Transporters / metabolism
  • Sweat / chemistry

Substances

  • Aminophenols
  • Aminopyridines
  • Antiporters
  • Benzodioxoles
  • CFTR protein, human
  • Chloride Channel Agonists
  • Quinolones
  • SLC26A9 protein, human
  • Sulfate Transporters
  • Cystic Fibrosis Transmembrane Conductance Regulator
  • ivacaftor
  • lumacaftor