CFTR modulates aquaporin-mediated glycerol permeability in mouse Sertoli cells

• Type: Article in International Scientific Journal
• Date: 2022

Authors

Ribeiro, JC (Author) Other; Bernardino, RL (Author) ICBAS; Carrageta, DF (Author) Other; Soveral, G (Author) Other; Calamita, G (Author) Other; Alves, MG (Author) Other; Oliveira, PF (Author) Other

Journal

Title: Cellular and Molecular Life Sciences

Vol. 79

ISSN: 1420-682X

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 0 Citations

Scopus

Other information

Authenticus ID: P-00X-ES1

DOI: 10.1007/s00018-022-04619-1

Abstract (EN): The cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel that is crucial for fluid homeodynamics throughout the male reproductive tract. Previous evidence shed light on a potential molecular partnership between this channel and aquaporins (AQPs). Herein, we explore the role of CFTR on AQPs-mediated glycerol permeability in mouse Sertoli cells (mSCs). We were able to identify the expression of CFTR, AQP3, AQP7, and AQP9 in mSCs by RT-PCR, Western blot, and immunofluorescence techniques. Cells were then treated with CFTRinh-172, a specific CFTR inhibitor, and its glycerol permeability was evaluated by stopped-flow light scattering. We observed that CFTR inhibition decreased glycerol permeability in mSCs by 30.6% when compared to the control group. A DUOLINK proximity ligation assay was used to evaluate the endogenous protein-protein interactions between CFTR and the various aquaglyceroporins we identified. We positively detected that CFTR is in close proximity with AQP3, AQP7, and AQP9 and that, through a possible physical interaction, CFTR can modulate AQP-mediated glycerol permeability in mSCs. As glycerol is essential for the control of the blood-testis barrier and elevated concentration in testis results in the disruption of spermatogenesis, we suggest that the malfunction of CFTR and the consequent alteration in glycerol permeability is a potential link between male infertility and cystic fibrosis.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 12