Expression of vascular endothelial growth factor and its receptors in infertile men with varicocele

An enlargement of the spermatic vein is known as a varicocele. Research studies suggest that immune system mediators such as vascular endothelial growth factor (VEGF) and its receptors including VEGFR1, VEGFR2, and VEGFR3 can play a role in angiogenesis and inhibition of endothelial cell apoptosis and correspondingly suppress spermatogenesis. Thus, the purpose of this study was to measure the expression of VEGF and its receptors in infertile men with varicocele.

To meet the research objectives, a total number of 30 infertile male patients affected with varicocele (Grade 3) and 30 healthy fertile male subjects without any varicocele or urogenital tract disorder were enrolled in the study. The varicose and normal veins were obtained from the patients along with the blood flowing in these spermatic veins during surgery. Also, peripheral blood samples were collected from the mentioned patients and healthy subjects. The serum levels of VEGF were also measured via enzyme-linked immunosorbent assay (ELISA) and subsequently mRNA level of VEGFR1, VEGFR2, VEGFR3, B Cell Lymphoma-Associated X (Bax), and B-cell lymphoma 2 (Bcl2) genes were measured using the real-time polymerase chain reaction (RT-PCR) technique.

The findings of this study revealed that VEGFR2 gene expression in varicose veins was significantly increased compared with normal veins in varicocele patients (P < 0.001) and Bax/Bcl2 ratio reduced in varicose veins when compared to normal veins of the patients (P < 0.05). Our findings also showed a significant rise in the serum levels of VEGF in the peripheral blood and varicose vein bloodstream compared with those in healthy subjects (P < 0.0001). Moreover, a significant difference was observed in the serum levels of VEGF in the peripheral blood and varicose vein blood of patients suffering from varicocele (P < 0.001).

According to the results of this study, VEGF/VEGFR2 axis might act in the survival of endothelial cells of varicocele vein through inhibition of apoptosis and stimulation of angiogenesis. Additionally, increased VEGF in the testis can probably play a role in suppressing spermatogenesis and varicocele-based infertility.