[Impacts of ODF2 gene knockdown on the sperm motility and fertility of male mice].

OBJECTIVE: To investigate the knockdown of the outer dense fiber protein 2 (ODF2) gene on the sperm motility and fertility of male mice. METHODS: We constructed three knockdown vectors with the target gene ODF2 and one control vector without the target gene. After infecting ICR mice, we determined the vector with the best knockdown effect by RT-PCR and Western blot and reinfected the mice with it. Then we obtained and analyzed the sperm motility parameters, pathological changes of the testis issue, and the litter size of the mice with gene knockdown. RESULTS: Compared with the normal controls, the mice infected with the vector with the best knockdown effect showed significantly decreased sperm motility parameters, pathomorphological abnormalities of the testis, and a reduced litter size (10.86 ± 1.28 vs 12.72 ± 2.05, P = 0.001). CONCLUSION: Decreased expression of the ODF2 gene deceases sperm motility parameters, impairs the morphology of the testis and affects the fertility of male mice.

[Expressions of ODF2 mRNA and protein are down-regulated in the sperm of asthenospermia patients].

OBJECTIVE: To investigate the mRNA and protein expressions of outer dense fiber 2 (ODF2) in the sperm of the asthenospermia patient and their differences from those in normal healthy men. METHODS: According to the WHO criteria, we collected semen samples from 45 asthenozoospermia patients and 15 normal healthy volunteers. Using computer-assisted sperm analysis (CASA), we divided the semen samples from the asthenospermia patients into a mild, a moderate and a severe group, and determined the mRNA and protein expressions of ODF2 in different groups by RT-PCR and Western blot. RESULTS: Compared with the normal healthy men, the expression of the ODF2 gene showed no statistically significant difference in the mild asthenospermia group (1.112 0 ± 0.525 5 vs 0.688 0 ± 0.372 0, P >0.05) but remarkably decreased in the moderate (0.483 3 ± 0.186 3, P <0.05) and severe asthenospermia patients (0.448 3 ± 0.340 8, P <0.01). The OD value (ODF2/ß-actin) of the ODF2 protein in the normal men exhibited no statistically significant difference from that in the mild asthenospermia group (0.458 7 ± 0.052 1 vs 0.326 1 ± 0.071 4, P >0.05), but markedly lower than in the moderate (0.145 4 ± 0.053 6, P <0.05) and severe asthenospermia patients (0.122 7 ± 0.045 7, P <0.01), which was consistent with the results of RT-PCR. CONCLUSIONS: Decreased mRNA and protein expressions of ODF2 in the sperm are positively correlated with declined sperm motility of the asthenospermia patient, which is suggestive of the involvement of the ODF2 gene in the regulation of sperm motility.