Organ-specific production control of vascular endothelial growth factor in ovarian hyperstimulation syndrome-model rats

Overproduction of vascular endothelial growth factor (VEGF) following human chorionic gonadotropin (hCG) stimulation has been implicated as one of the causative factors in the development of ovarian hyperstimulation syndrome (OHSS). The objective of this study was to clarify the action of hCG and progesterone, one of the possible factors for OHSS, on VEGF production and gene expression using OHSS-model rats. A total of 40 immature female Wistar rats were stimulated with 10 IU of equine chorionic gonadotropin for four consecutive days from the 22nd to 25th day of life followed by subcutaneous injection of 30 IU of hCG on the 26th day of life. RU486 and progesterone were injected 24 h after the hCG injection. Tissues and blood samples were collected on the 28th day. hCG elicited VEGF production in the OHSS-model rat ovaries. Ovarian weights of the OHSS model rats were significantly increased through day 26 by the ovarian stimulation with single dose of 30 IU hCG. Addition of anti-progesterone RU486, which reduced the ovarian enlargement, attenuated VEGF production dose dependently whereas the VEGF gene expression was stable. In the lung and liver, neither hCG nor RU486 affected VEGF production and gene expression. These results suggested that progesterone regulates VEGF production at the post-transcriptional level in a tissue specific manner in the hyperstimulated ovary.