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Seminal fluid extracellular vesicles restore human sperm osmoregulation after
cystic fibrosis transmembrane conductance regulator inhibition
#MMPMID41381597
Pereira SC
; Fomichova O
; Damião I
; Oliveira S
; Almeida V
; Monteiro MP
; Sousa M
; Bernardino RL
Sci Rep
2025[Dec]; 15
(1
): 43627
PMID41381597
show ga
Cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel
that promotes the exchange of chloride (Cl(-)) and bicarbonate (HCO(3)(-)),
modulating the balance of ions and water in various tissues. CFTR is also
expressed in the equatorial region of the spermatozoa's head. However, the
modulation of ionic and water transport via CFTR in spermatozoa needs further
investigation. To better understand how CFTR participates in the molecular
mechanisms behind spermatozoa modulation of water transport, and its impact on
sperm physiology, CFTR function of human spermatozoa was inhibited with 20 µM
CFTR(Inh)-172. The inhibition of CFTR promoted a decrease in intracellular
[Cl(-)] and membrane glycerol/water permeability, without any impact on sperm
vitality or off-target effect in Ca(2+) channels (assessed through the evaluation
of intracellular [Ca(2+)]). To reverse the effects of CFTR inhibition, we
incubated spermatozoa with CFTR-carrying seminal fluid extracellular vesicles
(SF-EVs). We reported that the SF-EVs were able to restore the CFTR activity of
spermatozoa previously exposed to the inhibitor, characterized by a restoration
of Cl(-), glycerol/water permeability, and a recovery of sperm osmoregulation
capacity. Our results provide evidence for the important role of CFTR function in
sperm osmoregulation and suggest that the use of CFTR-containing EVs - already
employed in the treatment of cystic fibrosis - could be explored to enhance sperm
quality.
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