Steroid-Induced Final Maturation in Brook Trout (Salvelinus Fontinalis) Oocytes in Vitro: The Effects of Forskolin and Phosphodiesterase Inhibitors1

DeManno, Deborah A.; Goetz, Frederick W.

doi:10.1095/biolreprod36.5.1321

Cited by 46 publications

(18 citation statements)

References 31 publications

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“…Further, the PDE inhibitors IBMX, theophylline and caffeine also inhibited the 2-OHE 2 -induced GVBD. The response of the PDE inhibitors appears to vary with species, inhibitor type and concentration and duration (DeManno and Goetz, 1987a;DeManno and Goetz, 1987b;Chaube and Haider, 1997;Haider and Baqri, 2000;Pace and Thomas, 2005). In the present study, the inhibitory response was evident at >0.1·mmol·l -1 for IBMX, >0.5·mmol·l -1 for theophylline and at >1.0·mmol·l -1 for caffeine in the co-incubation studies.…”

Section: Discussionsupporting

confidence: 51%

“…The adenylyl cyclase activator forskolin, which stimulates cAMP, has been demonstrated to inhibit MIS-induced maturation in fish (see Jalabert et al, 1991;Haider and Chaube, 1995). Likewise, the PDE inhibitors, such as IBMX and theophylline that elevate cAMP, have been shown to inhibit the MIS-induced maturation (DeManno and Goetz, 1987a;DeManno and Goetz, 1987b;Chaube and Haider, 1997;Haider and Baqri, 2000). Haider and Baqri (Haider and Baqri, 2000) showed a correlation between PDE activity, cAMP level and GVBD response.…”

Section: Discussionmentioning

confidence: 99%

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2-hydroxyestradiol-17β-induced oocyte maturation: involvement of cAMP–protein kinase A and okadaic acid-sensitive protein phosphatases,and their interplay in oocyte maturation in the catfishHeteropneustes fossilis

Mishra

Joy

2006

Journal of Experimental Biology

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SUMMARY In Heteropneustes fossilis, in vitro incubation of postvitellogenic follicles with 2-hydroxyestradiol-17β(2-OHE2, 5 μmol l–1) decreased significantly the total cAMP level, concomitant with germinal vesicle breakdown (GVBD). The incubation of the follicles with cAMP or cAMP-elevating drugs[phosphodiesterase (PDE) inhibitors], such as IBMX(3-isobutyl-1-methyl-xanthine), theophylline and caffeine, inhibited the 2-OHE2-induced GVBD in a concentration-dependent manner. The magnitude of the response varied: both cAMP and IBMX were effective at all concentrations (0.1–2.0 mmol l–1), followed by theophylline (0.5–2.0 mmol l–1) and caffeine(1–2.0 mmol l–1). The protein kinase A (PKA) inhibitor H89 stimulated oocyte maturation in a concentration-dependent manner. However,when co-incubated with 2-OHE2 for 24 h it produced a biphasic effect: low concentrations (0.1 and 1.0 μmol l–1) did not alter the 2-OHE2-induced GVBD, but high concentrations (5 and 10μmol l–1) inhibited it. The incubation of the follicles with H89 lowered the inhibitory effect of IBMX on the 2-OHE2-induced GVBD. The incubation of the follicles with okadaic acid (OA), a protein phosphatase 1 and 2A inhibitor did not affect GVBD but when co-incubated with 2-OHE2, it enhanced the GVBD response. OA reversed the inhibitory effect of IBMX. The results suggest that OA may overcome the inhibition of 2-OHE2-induced GVBD by IBMX at a step distal to the cAMP–PKA pathway.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

2-hydroxyestradiol-17β-induced oocyte maturation: involvement of cAMP–protein kinase A and okadaic acid-sensitive protein phosphatases,and their interplay in oocyte maturation in the catfishHeteropneustes fossilis

Mishra

Joy

2006

Journal of Experimental Biology

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“…In teleosts, high intra-oocyte cAMP is considered as a pre-requisite for prophase-I arrest and attenuate MIS action on OM in a variety of teleosts species (DeManno & Goetz 1987, Haider & Baqri 2002). Next we examined effects of Ac inhibition or cAMP modulators on spontaneous maturation and DHP/Igf1-mediated GVBD response.…”

Section: Effect Of Camp/pka Regulation Of Dhp And/or Igf1 Induced Meimentioning

confidence: 99%

Releasing prophase arrest in zebrafish oocyte: synergism between maturational steroid and Igf1

Das¹,

Pal²,

Maitra³

2016

Reproduction

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Binding of 17b-estradiol (E 2 ) to novel G-protein coupled receptor, Gper1, promotes intra-oocyte adenylyl cyclase activity and transactivates epidermal growth factor receptor to ensure prophase-I arrest. Although involvement of either membrane progestin receptor (mPR) or Igf system has been implicated in regulation of meiosis resumption, possibility of concurrent activation and potential synergism between 17a,20b-dihydroxy-4-pregnen-3-one (DHP)-and Igf-mediated signalling cascades in alleviating E 2 inhibition of oocyte maturation (OM) has not been investigated. Here using zebrafish (Danio rerio) defolliculated oocytes, we examined the effect of DHP and Igf1, either alone or in combination, in presence or absence of E 2 , on OM in vitro. While priming of denuded oocytes with E 2 blocked spontaneous maturation, co-treatment with DHP (3 nM) and Igf1 (10 nM), but not alone, reversed E 2 inhibition and promoted a robust increase in germinal vesicle breakdown (GVBD). Although stimulation with either Igf1 or DHP promoted Akt phosphorylation, pharmacological inhibition of PI3K/Akt signalling prevented Igf1-induced GVBD but delayed DHP action till 4-5 h of incubation. Moreover, high intra-oocyte cAMP attenuates both DHP and Igf1-mediated OM and co-stimulation with DHP and Igf1 could effectively reverse E 2 action on PKA phosphorylation. Interestingly, data from in vivo studies reveal that heightened expression of igf1, igf3 transcripts in intact follicles corresponded well with elevated phosphorylation of Igf1r and Akt, mPRa immunoreactivity, PKA inhibition and accelerated GVBD response just prior to ovulation. This indicates potential synergism between maturational steroid and Igf1 which might have physiological relevance in overcoming E 2 inhibition of meiosis resumption in zebrafish oocytes.

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“…Activation of Gper on Atlantic croaker and zebrafish oocytes by estradiol-17b (E 2 ) or the specific GPER agonist, G-1, blocks spontaneous meiotic maturation of denuded oocytes and attenuates induction of oocyte maturation (OM) by the maturationinducing steroid (Pang et al 2008, Pang & Thomas 2009. These inhibitory actions of estrogens on OM are partially mediated through activation of membrane adenylyl cyclase to sustain high cAMP concentrations in the oocyte, which are essential for maintaining meiotic arrest (DeManno & Goetz 1987, Pang et al 2008. They may also involve Egfr and Mapk3/1 because these inhibitory effects were blocked by co-treatment with several specific inhibitors of the EGFR pathway and MAPK (Peyton & Thomas 2011).…”

Section: Introductionmentioning

confidence: 99%

Role of Pgrmc1 in estrogen maintenance of meiotic arrest in zebrafish oocytes through Gper/Egfr

Aizen¹,

Thomas²

2015

Journal of Endocrinology

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The regulation of receptor trafficking to the cell surface and its effect on responses of target cells to growth factors and hormones remain poorly understood. Initial evidence has been recently obtained using cancer cells that surface expression of the epidermal growth factor receptor (EGFR) is dependent on its association with progesterone receptor membrane component 1 (PGRMC1). Estrogen inhibition of oocyte maturation (OM) in zebrafish is mediated through G-protein-coupled estrogen membrane receptor 1 (Gper1) and involves activation of Egfr. Therefore, in this study, the potential roles of Pgrmc1 in the cell surface expression and functions of Egfr in normal cells were investigated in this in vitro OM model of Egfr action using an inhibitor of PGMRC1 signaling, AG205. A single w60 kDa protein band, which corresponds to the size of the Pgrmc1 dimer, was detected on plasma membranes of fully grown oocytes by western blotting. Co-treatment with the PGRMC1 inhibitor AG205 (20 mM) blocked the inhibitory effects of 100 nM estradiol-17b and the GPER agonist, G-1, on spontaneous maturation of denuded zebrafish oocytes. Moreover, reversal of these estrogen effects on OM by the EGFR inhibitors AG1478 and AG825 (50 mM) was prevented by co-incubation with the PGRMC1 inhibitor. Inhibition of Pgrmc1 signaling with AG205 also caused a decrease in Egfr-dependent signaling and Egfr expression on oocyte cell membranes. These results indicate that maintenance of Pgrmc1 signaling is required for Egfr expression on zebrafish oocyte cell membranes and for conserving the functions of Egfr in maintaining meiotic arrest through estrogen activation of Gper.

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Steroid-Induced Final Maturation in Brook Trout (Salvelinus Fontinalis) Oocytes in Vitro: The Effects of Forskolin and Phosphodiesterase Inhibitors1

Cited by 46 publications

References 31 publications

2-hydroxyestradiol-17β-induced oocyte maturation: involvement of cAMP–protein kinase A and okadaic acid-sensitive protein phosphatases,and their interplay in oocyte maturation in the catfishHeteropneustes fossilis

2-hydroxyestradiol-17β-induced oocyte maturation: involvement of cAMP–protein kinase A and okadaic acid-sensitive protein phosphatases,and their interplay in oocyte maturation in the catfishHeteropneustes fossilis

Releasing prophase arrest in zebrafish oocyte: synergism between maturational steroid and Igf1

Role of Pgrmc1 in estrogen maintenance of meiotic arrest in zebrafish oocytes through Gper/Egfr

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