Table 3 - uploaded by Lloyd Lee Anderson
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1 Accession number, gene, primer sequences (forward and reverse primers; 5' to 3') and location of the primers within the GenBank sequence for PCR amplifications.
Citations
... To this aim, the present in vivo study was designed to study the effects induced by P 4 antagonist administration, RU486 [48][49][50][51][52][53], on VEGF expression and angiogenesis during the transition from preovulatory to periovulatory follicles in gilts. This phase of follicle development was in vivo reproduced using a validated hormonal protocol [7,27] able to promote antral follicular growth until the preovulatory stage (eCG injection) and ovulation (hCG treatment). ...
... Our results demonstrate, for the first time, that VEGF production, blood vessel network, and follicle tissue remodeling were all affected by the in vivo administration of RU486 during the phase of transition from pre to periovulatory follicle, characterized by increasing levels of P 4 [28,29], even if the cause-effect correlation between these events remains to be clarified. In addition to pregnancy [52,53,58,59], ovulation [60][61][62][63][64][65], and sperm-oocyte recognition [66], a new RU486 negative effect was demonstrated on reproductive events. Indeed, RU486 administration was able to impair periovulatory follicle development and angiogenesis induced by hCG. ...
The success of ovarian follicle growth and ovulation is strictly related to the development of an adequate blood vessel network required to sustain the proliferative and endocrine functions of the follicular cells. Even if the Vascular Endothelial Growth Factor (VEGF) drives angiogenesis before ovulation, the local role exerted by Progesterone (P4) remains to be clarified, in particular when its concentration rapidly increases before ovulation.
This in vivo study was designed to clarify the effect promoted by a P4 receptor antagonist, RU486, on VEGF expression and follicular angiogenesis before ovulation, in particular, during the transition from pre to periovulatory follicles induced by human Chorionic Gonadotropins (hCG) administration.
Preovulatory follicle growth and ovulation were pharmacologically induced in prepubertal gilts by combining equine Chorionic Gonadotropins (eCG) and hCG used in the presence or absence of RU486. The effects on VEGF expression were analyzed using biochemical and immunohistochemical studies, either on granulosa or on theca layers of follicles isolated few hours before ovulation. This angiogenic factor was also correlated to follicular morphology and to blood vessels architecture.
VEGF production, blood vessel network and follicle remodeling were impaired by RU486 treatment, even if the cause-effect correlation remains to be clarified. The P4 antagonist strongly down-regulated theca VEGF expression, thus, preventing most of the angiogenic follicle response induced by hCG. RU486-treated follicles displayed a reduced vascular area, a lower rate of endothelial cell proliferation and a reduced recruitment of perivascular mural cells. These data provide important insights on the biological role of RU486 and, indirectly, on steroid hormones during periovulatory follicular phase. In addition, an in vivo model is proposed to evaluate how periovulatory follicular angiogenesis may affect the functionality of the corpus luteum (CL) and the success of pregnancy.
... Moreover, PGR is a nuclear receptor that acts as a transcription factor to mediate the LH ovulatory response by the expression of key genes such as ADAMTS1 and Catepsin L [151] for reviews [87,125,152153154 . The inhibition of PGR or progesterone action prevents meiosis resumption and ovulation in pig [155,156]. Moreover the PRKO mice are unable to spontaneously ovulate, but when the oocytes are punctured and collected prior to ovulation, they are able to reach the blastocyst stage [154,157,158]. ...
The use of gonadotropins to trigger oocyte maturation both in vivo and in vitro has provided precious and powerful knowledge that has significantly increased our understanding of the ovarian function. Moreover, the efficacy of most assisted reproductive technologies (ART) used in both humans and livestock species relies on gonadotropin input, mainly FSH and LH. Despite the significant progress achieved and the huge impact of gonadotropins, the exact molecular pathways of the two pituitary hormones, FSH and LH, still remain poorly understood. Moreover, these pathways may not be the same when moving from the in vivo to the in vitro context. This misunderstanding of the intricate synergy between these two hormones leads to a lack of consensus about their use mainly in vitro or in ovulation induction schedules in vivo. In order to optimize their use, additional work is thus required with a special focus on comparing the in vitro versus the in vivo effects. In this context, this overview will briefly summarize the downstream gene expression pathways induced by both FSH in vitro and LH in vivo in the cumulus compartment. Based on micro array recent comparative analysis, we are reporting that in vitro FSH stimulation on cumulus cells appears to achieve at least part of the gene expression activity after in vivo LH stimulation. We are then proposing that the in vitro FSH-response of cumulus cells have similitudes with the in vivo LH-response.
