Effect of GnRH antagonist-induced prolonged follicular phase on follicular atresia and oocyte developmental competence in vitro in superovulated heifers

Oussaid, B.; Lonergan, P.; Khatir, H.; Güler, Ayşe; Monniaux, Danielle; Touzé, Jean-Luc; Beckers, J. F.; Cognie, Y.; Mermillod, Pascal

doi:10.1530/jrf.0.1180137

Cited by 23 publications

(8 citation statements)

References 6 publications

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“…The maintenance of the preovulatory follicles in superovulated heifers with GnRH-ant is detrimental to follicular health, inducing high concentrations of atresia and a decrease in FF E 2 and progesterone concentrations [51]. We believe that ovary cells may counter apoptosis, as happens in many other organs, by secreting and releasing IGF-I.…”

Section: Discussionmentioning

confidence: 89%

Gonadotropin-releasing hormone antagonists increase follicular fluid insulin-like growth factor-I and vascular endothelial growth factor during ovarian stimulation cycles

Ferrari

Pezzuto

Barusi

et al. 2006

Gynecological Endocrinology

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The aim of the present study was to investigate the effect of gonadotropin-releasing hormone (GnRH) antagonists (GnRH-ant) on follicular fluid (FF) insulin-like growth factor-I (IGF-I) and FF vascular endothelial growth factor (VEGF) levels. Sixty women undergoing assisted reproduction were randomized and assigned to two different GnRH analog regimens: GnRH agonist (GnRH-a) and GnRH-ant. FF VEGF and FF IGF-I concentrations were significantly increased in the patients treated with GnRH-ant (p < 0.001). In the same patients we observed a statistically significant reduction in serum luteinizing hormone (LH) and estradiol (E2) levels (p < 0.001 and p < 0.05, respectively), FF E2 and FF androstenedione levels (p < 0.05 and p < 0.001, respectively), as well as a reduction in the number of pregnancies although this was not statistically significant. In the GnRH-ant group, FF VEGF levels were positively correlated with FF IGF-I levels, and both were negatively correlated with serum LH levels. The increase in FF IGF-I and FF VEGF levels in women treated with GnRH-ant could be explained by a deleterious follicular environment in response to profound suppression of LH and E2 levels.

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Section: Discussionmentioning

confidence: 89%

Gonadotropin-releasing hormone antagonists increase follicular fluid insulin-like growth factor-I and vascular endothelial growth factor during ovarian stimulation cycles

Ferrari

Pezzuto

Barusi

et al. 2006

Gynecological Endocrinology

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“…In other words, it represents an ''intrafollicular oocyte aging'' after ovulation stimulation. This type of preovulatory oocyte aging can be induced by treatment of females with a sodium pentobarbital [18], a gonadotropin-releasing hormone antagonist [19], some progestins [20], or inosine monophosphate dehydrogenase inhibitors [21]. It is quite different from the concept of preovulatory oocyte aging with maternal aging, and is rather similar to postovulatory oocyte aging.…”

Section: Defining Oocyte Agingmentioning

confidence: 99%

Cellular and molecular mechanisms of various types of oocyte aging

Takahashi

Igarashi

Amita

et al. 2011

Reprod Medicine & Biology

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It is well established that age-related decline of a woman's fertility is related to the poor developmental potential of her gametes. The age-associated decline in female fertility is largely attributable to the oocyte aging caused by ovarian aging. Age-associated oocyte aging results in a decrease in oocyte quality. In contrast to ovarian aging, there is a concept of postovulatory oocyte aging. Postovulatory aging of oocytes, not being fertilized for a prolonged time after ovulation, is known to significantly affect the development of oocytes. Both categories of oocyte aging have similar phenotypes of reproductive failure. However, the mechanisms of the decline in oocyte quality are not necessarily equivalent. An age-dependent increase in aneuploidy is a key determinant of oocyte quality. The reduced expression of molecules regulating cell cycle control during meiosis might be involved in the age-dependent increase in aneuploidy. The mechanism of age-associated oocyte aging might be involved in mitochondrial dysfunction, whose etiologies are still unknown. Alternatively, the mechanism of postovulatory oocyte aging might be involved in reactive oxygen species-induced mitochondrial injury pathways followed by abnormal intracellular Ca regulation of the endoplasmic reticulum. We suggest that future research into the mechanism of oocyte aging will be necessary to develop a method to rescue the poor developmental potential of aged oocytes.

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“…1999). Interestingly, when atresia was induced by prolonged follicular phase under gonadotropin suppression in superovulated heifers, oocyte quality was not affected (Oussaid et al. 2000).…”

Section: Oocyte Differentiation In Vivomentioning

confidence: 99%

Factors Affecting Oocyte Quality: Who is Driving the Follicle?

Mermillod

Dalbiès-Tran

Uzbekova

et al. 2008

Reprod Domestic Animals

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Mammalian ovaries contain a large stock of oocytes enclosed in primordial follicles. Ovarian cyclic activity induces some of these follicles to initiate growth towards a possible ovulation. However, most of these follicles terminate their growth at any moment and degenerate through atresia. In growing follicles, only a subset of oocytes are capable to support meiosis, fertilization and early embryo development to the blastocyst stage, as shown through embryo in vitro production experiments. This proportion of competent oocytes is increasing along with follicular size. Growing lines of evidence suggest that oocyte competence relies on the storage of gene products (messenger RNA or protein) that will be determinant to support early stages of embryo development, before full activation of embryonic genome. Given these facts, the question is: are these gene products stored in oocytes during late folliculogenesis, allowing an increasing proportion of them to become competent? Alternatively, these transcripts may be stored during early folliculogenesis as the oocyte grows and displays high transcription activity. Several arguments support this latter hypothesis and are discussed in this review: (i) many attempts at prolonged culture of oocytes from antral follicles have failed to increase developmental competence, suggesting that developmental competence may be acquired before antral formation; (ii) the recent discovery of oocyte secreted factors and of their ability to regulate many parameters of surrounding somatic cells, possibly influencing the fate of follicles between ovulation or atresia, suggests a central role of oocyte quality in the success of folliculogenesis. Finally, in addition to their role in interfollicular regulation of ovulation rate, late folliculogenesis regulation and atresia could also be seen as a selective process aimed at the elimination through follicular atresia of oocytes that did not succeed to store proper gene products set during their growth.

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Effect of GnRH antagonist-induced prolonged follicular phase on follicular atresia and oocyte developmental competence in vitro in superovulated heifers

Cited by 23 publications

References 6 publications

Gonadotropin-releasing hormone antagonists increase follicular fluid insulin-like growth factor-I and vascular endothelial growth factor during ovarian stimulation cycles

Gonadotropin-releasing hormone antagonists increase follicular fluid insulin-like growth factor-I and vascular endothelial growth factor during ovarian stimulation cycles

Cellular and molecular mechanisms of various types of oocyte aging

Factors Affecting Oocyte Quality: Who is Driving the Follicle?

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