Increased expression of vascular endothelial growth/permeability factor in the rat ovary following an ovulatory gonadotropin stimulus: potential roles in follicle rupture

Abstract

Ovulation is accompanied by a large increase in the permeability of the capillaries surrounding the follicle, beginning a few hours after the ovulatory stimulus. The resulting edema may play a role in ovulation as well as in the formation and vascularization of the CL. Vascular endothelial growth/permeability factor (VEG/PF) is both a specific mitogen for endothelial cells and a potent stimulator of vascular permeability. The purpose of this study was to determine whether or not the ovulatory stimulus induces an increase in the expression of VEG/PF in the ovary. Female rats were primed with 8 IU of eCG at 27 days of age. Follicular maturation and ovulation were induced with an injection of hCG (5 IU) in the early afternoon on the second day after priming. Ovaries were removed 0, 1, 2, 4, 8, 10, and 18 h later. VEG/PF mRNA levels were compared through use of quantitative reverse transcription-polymerase chain reaction (RT-PCR). There was a marked increase (approximately 8-fold) in steady state levels of the transcripts for VEG/PF120 and VEG/PF164 between 1 and 4 h after hCG in whole ovaries. Increases were detectable both in granulosa cells and in thecal/stromal tissue. The high level of expression was maintained at 10 and 18 h (Day 1 CL). Thus, the preovulatory increase in follicular vascular permeability is closely associated with a marked, sustained increase in VEG/PF expression. VEG/PF, therefore, may play an important role in that increase and, consequently, in the process of ovulation as well as the subsequent vascularization of the CL.

Immunolocalization of von Willebrand Factor and Vascular Endothelial Growth Factor during Follicular Atresia in the Swamp Buffalo Ovary

“…This localization was high in the granulosa of healthy follicles in SB and HF. A similar observation was noted in bovine [36] and rat [37] ovarian follicles. These previous studies also noted that an increased ligand expression resulted in enhanced capillary proliferation.…”

Short oestrous cycles in sheep during anoestrus involve defects in progesterone biosynthesis and luteal neovascularisation

“…Modulation of angiogenesis during the luteal phase by Luteal failure and the short cycle in ewes treatment with inhibitors of VEGFA signalling either at or shortly following ovulation significantly reduced the number of proliferative and endothelial cells within the CL and significantly decreased progesterone secretion (Wulff et al 2001c, Hazzard et al 2002, while a more prolonged treatment, well into the luteal phase, resulted in a complete ablation of microvascular branching (Wulff et al 2001a(Wulff et al , 2001b. Inhibition of LH signalling using GNRH antagonists mimicked this effect, also suppressing early luteal angiogenesis and implicating the LH surge in normal luteal angiogenesis, consistent with the described induction of VEGFA signalling by LH (Koos 1995, Dickson & Fraser 2000. The in vivo inhibition of VEGFA signalling throughout the luteal phase (days 3-10 in the marmoset monkey) also decreased luteal angiogenesis and the blood concentration of progesterone (Dickson et al 2001, Wulff et al 2001c.…”

Expression and contribution of the HIF‑1α/VEGF signaling pathway to luteal development and function in pregnant rats

“…Hypoxia is a potent stimulus for the expression of VEGF (14,23), as ovulation causes a decline of local oxygen concentration, producing a hypoxic environment, and may be the predominant stimulator for VEGF production in the developing corpus luteum (5,24). However, there have been no reports regarding the contribution of HIF-1α signaling to VEGF-dependent angiogenesis and luteal function during ovarian luteal formation in vivo.…”