Ultrasound-targeted microbubble destruction disrupts the blood-testis barrier

Ultrasound-targeted microbubble disruption (UTMD) has caused significant concern with regard to opening the blood-testis barrier (BTB), yet the mechanism of how UTMD opens the BTB has not yet been fully clarified. The main mechanisms of UTMD are the cavitation effect, acoustic pore effect, alteration of cellular membrane permeability and stimulation of cellular endocytosis, which can significantly affect the BTB. The objective of this study was to investigate the effect of UTMD on BTB function and determine whether it affects BTB function via noncollagenous 1 (NC1) peptide and apical ectoplasmic specialization-blood-testis barrier-basement membrane (apical ES-BTB-BM).

Adult male rats were given ultrasound irradiation, low-concentration UTMD (UTMD-low) or high-concentration UTMD (UTMD-high) irradiation for 150 s, with the rats euthanized 0, 6, 24 and 72 h later. The effects of UTMD on BTB permeability were verified using a BTB permeability assay, immunofluorescence, quantitative PCR and immunoblot.

UTMD increased the RNA level of NC1, decreased the protein expression of EB1 and altered the structure of End-binding protein 1 (EB-1); organization of actin-related protein 3 (Arp3), F-actin and α-tubulin was also damaged. In addition, UTMD caused BTB in adult rats, with more pronounced UTMD-high damage to the BTB.

These findings suggest that NC1, EB-1, Arp3, F-actin and α-tubulin may be involved in the process of BTB damage by UTMD in adult male rats. Therefore, UTMD damage to the BTB may be mediated by elevating the RNA level of NC1, decreasing the expression of EB1 and altering the organization of EB-1, Arp3, F-actin and α-tubulin.