Maturational Effects of Gonadotropins on the Cumulus-Oocyte Complex of the Rat

Dekel, Nava; Hillensjø, Torbjörn; Kraicer, P. F.

doi:10.1095/biolreprod20.2.191

Cited by 101 publications

(42 citation statements)

References 17 publications

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“…Angiotensin II in bovine oocyte meiosis resumption inhibited the meiotic resumption induced by LH surge; 2) the nonselective PTGS inhibition blocked AngII-induced meiotic resumption of bovine oocytes co-cultured with follicular hemisections and 3) the addition of PGE 2 or PGF 2a into an in vitro co-culture system of oocytes and follicular cells resulted in the same pattern of meiotic resumption induced by AngII. Resumption of meiosis in fully grown follicles is triggered by a preovulatory surge of LH (Ayalon et al 1972, Dekel et al 1979, and herein we report the inhibition of these events by a competitive AngII antagonist. These results are complementary to previous findings of our group regarding oocyte meiotic resumption (Giometti et al 2005, Stefanello et al 2006) and ovulation, an event closely related to oocyte maturation (Ferreira et al 2007).…”

Section: Discussionmentioning

confidence: 58%

Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E2 and F2α

Barreta

Oliveira²,

Ferreira³

et al. 2008

Reproduction

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Angiotensin II (AngII) prevents the inhibitory effect of follicular cells on oocyte maturation, but its involvement in LH-induced meiotic resumption remains unknown. The aim of this study was to assess the involvement of AngII in LH-induced meiotic resumption and of prostaglandins (PGs) in the action of AngII. In the experiment I, seven cows were superovulated, intrafollicularly injected with 10 mM saralasin (a competitive AngII antagonist) or saline when the follicles reached a diameter larger than 12 mm, and challenged with a GnRH agonist to induce an LH surge. Fifteen hours after GnRH, the animals were ovariectomized and the oocytes were recovered to determine the stage of meiosis. The oocytes from follicles that received saline were in germinal vesicle (GV) breakdown (30.8%) or metaphase I (MI; 69.2%) stage while those that received saralasin were in the GV stage (100%; P!0.001) 15 h after GnRH agonist. In another experiment, oocytes were co-cultured with follicular hemisections for 15 h to determine whether PGs mediate the effect of AngII on meiotic resumption. Indomethacin (10 mM) inhibited AngII-induced meiotic resumption (13.4 vs 77.5% MI without indomethacin; P!0.001). Furthermore, the GV oocytes progressed to MI at a similar rate when PGE 2 , PGF 2a or AngII was present in the co-culture system with follicular cells (PGE 2 77.4%, PGF 2a 70.0%, and AngII 75.0% MI). In conclusion, our results provide strong evidence that AngII mediates the resumption of meiosis induced by an LH surge in bovine oocytes and that this event is dependent on PGE 2 or PGF 2a produced by follicular cells. Reproduction (2008) 136 733-740

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Section: Discussionmentioning

confidence: 58%

Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E2 and F2α

Barreta

Oliveira²,

Ferreira³

et al. 2008

Reproduction

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“…Our collection of follicular fluid was complete by 3 h after slaughter with all but the first 20 min being carried out at <4°C. In contrast, in the report by Tsafriri & Channing (1975) (Dekel & Kraicer, 1978 ;Dekel, Hillensjo & Kraicer, 1979;Eppig, 1980) (Foote & Thibault, 1969;Leibfried & First, 1980b). Additional changes in the environment of the oocyte upon liberation in vitro include changes in pH, pC02 or p02.…”

Section: Discussionmentioning

confidence: 94%

Porcine follicular fluid does not inhibit maturation of rat oocytes in vitro

Fleming¹,

Khalil²,

Armstrong³

1983

Reproduction

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Summary. Follicular fluid from small-(1\p=n-\2mm) or medium-(3\p=n-\8mm) sized pig follicles was collected under conditions designed to minimize possible alteration or degradation of native fluid components. The effects of follicular fluid with or without benzamidine, an inhibitor of proteolytic activity, on oocytes collected 20 or 44 h after PMSG treatment of rats were examined. A follicular fluid fraction of Mr < 10 000 (PM-10 membrane filter) was also tested. Follicular fluid from small-and medium-sized follicles and control medium alone supported maturation of oocytes collected 20 or 44 h after PMSG, but follicular fluid (50%) from medium-sized follicles containing 5\m=.\0mm\ x=req-\ benzamidine significantly inhibited oocyte maturation. Comparable inhibition was also observed with medium containing 5\m=.\0mm-benzamidine. The PM-10 filtrate failed to inhibit oocyte maturation as assessed by germinal vesicle breakdown but did significantly inhibit first polar body formation and therefore restricted the extent of maturation. The results indicate that native pig follicular fluid is unable to inhibit the initiation of maturation of rat oocytes in vitro.

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“…For the experiments with the ROS scavengers, the samples were preincubated for 1.5 h with one of the following antioxidants: NAC (10 mM), BHA (125 μM), or GSH (40 mM) before the addition of LH or H 2 O 2 . COCs were recovered from the cultured follicles and microscopically examined for cumulus expansion as described previously (61). Progesterone concentrations were determined in the cultured medium according to a published procedure (62).…”

Section: Methodsmentioning

confidence: 99%

Reactive oxygen species are indispensable in ovulation

Shkolnik¹,

Tadmor²,

Ben‐Dor

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

312

213

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Ovulation is stimulated by the preovulatory surge of the pituitary luteinizing hormone (LH). Because the ovulatory response is commonly identified with inflammation, we explored the involvement of reactive oxygen species (ROS) in this process. Our experiments show that administration of broad-range scavengers of oxidative species into the ovarian bursa of mice, hormonally induced to ovulate, significantly reduced the rate of ovulation. LH-induced cumulus mucification/expansion, a necessary requirement for ovulation, was prevented by antioxidants both in vivo and in an ex vivo system of isolated intact ovarian follicles. Along this line, H 2 O 2 fully mimicked the effect of LH, bringing about an extensive mucification/expansion of the follicle-enclosed cumulusoocyte complexes. Impaired progesterone production was observed in isolated follicles incubated with LH in the presence of the antioxidant agents. Furthermore, LH-stimulated up-regulation of genes, the expression of which is crucial for ovulation, was substantially attenuated upon ROS ablation. This system was also used for demonstrating the role of ROS in phosphorylation and activation of the EGF receptor as well as its downstream effector, p42/44 MAPK. Together, our results provide evidence that ovarian production of ROS is an essential preovulatory signaling event, most probably transiently triggered by LH.ovary | cumulus expansion O vulation is an essential prelude for successful reproduction. The ovulatory process is initiated by the midcycle surge of the pituitary luteinizing hormone (LH) that induces substantial biochemical, molecular, and cellular changes, culminating in the release of a mature ovum surrounded by the cumulus cells (1). Before ovulation, the cumulus cells produce an extracellular, hyaluronan-rich matrix that brings about cumulus mucification and its expansion. This response to LH that is essential for ovulation (2) is subsequent to the expression of a set of specific genes (3) such as prostaglandin synthase 2 (Ptgs2) (4), hyaluronan synthase 2 (Has2) (5), tumor necrosis-stimulated gene 6 (Tnfaip6) (6), and CCAAT/enhancer-binding protein β (Cebpb), a downstream target of p42/44 MAPK (Erk1/2) (7). Also essential for ovulation is LH-induced progesterone receptor (Pgr) expression as well as progesterone production (8).Numerous genes related to inflammation are induced in preovulatory follicles by the LH surge (9-12). Moreover, ovulation is suppressed by agents that inhibit acute inflammatory reactions (13). The analogy of ovulation with an acute inflammation (9, 14) may suggest a role for reactive oxygen species (ROS) along this process. ROS originate from inflammatory cells, such as macrophages and neutrophils, which are massively recruited after the LH surge to the ovary (15), and their depletion impairs ovulation (16, 17). Cyclooxygenase 2 (Ptgs2), the expression of which is a hallmark for LHinduced ovulation, is associated with inflammation and generates ROS (18). ROS are also byproducts of monooxygenase reactions mediated by the P450...

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Maturational Effects of Gonadotropins on the Cumulus-Oocyte Complex of the Rat

Cited by 101 publications

References 17 publications

Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E2 and F2α

Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E2 and F2α

Porcine follicular fluid does not inhibit maturation of rat oocytes in vitro

Reactive oxygen species are indispensable in ovulation

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