Endocrine and paracrine regulation of meiotic cell cycle progression in teleost oocytes: cAMP at the centre of complex intra-oocyte signalling events

Das, Debabrata; Khan, Pragya Paramita; Maitra, Saumen Kumar

doi:10.1016/j.ygcen.2016.01.005

Cited by 33 publications

(32 citation statements)

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“…Cell proliferation and differentiation is a simultaneous and contradictory biological process. cAMP serves an important role in the regulation of these contradictions (41,42). To clarify how CD38 affects the concentration of cAMP in NPC cells, cAMP was tested and it was determined that the concentration of cAMP in 5-8F/CD38 cells was 60.25±3.23 ng/ml, and the 5-8F/Vector intracellular cAMP concentration was 53.48±2.49 ng/ml.…”

Section: Resultsmentioning

confidence: 99%

CD38 affects the biological behavior and energy metabolism of nasopharyngeal carcinoma cells

Long

Xiao

et al. 2018

Int J Oncol

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Nasopharyngeal carcinoma (NPC) is the most common malignant tumor type in Southern China and South-East Asia. Cluster of differentiation (CD)38 is highly expressed in the human immune system and participates in the activation of T, natural killer and plasma cells mediated by CD2 and CD3 through synergistic action. CD38 is a type II transmembrane glycoprotein, which was observed to mediate diverse activities, including signal transduction, cell adhesion and cyclic ADP-ribose synthesis. However, the significance of CD38 in NPC biological behavior and cellular energy metabolism has not been examined. In order to elucidate the effect of CD38 on the biological behavior of NPC cells, stable CD38-overexpressed NPC cell lines were established. It was demonstrated that CD38 promoted NPC cell proliferation with Cell Counting Kit-8 and colony formation assays. It was also indicated that CD38 inhibited cell senescence, and promoted cell metastasis. Furthermore, it was determined that CD38 promoted the conversion of cells to the S phase and decreased the content of reactive oxygen species and Ca2+. Additionally, cell metabolism assays demonstrated that CD38 increased the concentration of ATP, lactic acid, cyclic adenosine monophosphate and human ADP/acrp30 concentration in NPC cells. To investigate the possible mechanism, bioinformatics analysis and mass spectrometry technology was used to determine the most notably changing molecule and signaling pathways, and it was determined and verified that CD38 regulated the metabolic-associated signaling pathways associated with tumor protein 53, hypoxia inducible factor-1α and sirtuin 1. The present results indicated that CD38 may serve a carcinogenic role in NPC by regulating metabolic-associated signaling pathways.

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Section: Resultsmentioning

confidence: 99%

CD38 affects the biological behavior and energy metabolism of nasopharyngeal carcinoma cells

Long

Xiao

et al. 2018

Int J Oncol

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“…Insulin also induces GVBD in denuded (devoid of surrounding follicular cells) zebrafish oocytes, suggesting that insulin can mediate oocyte maturation via a pathway independent of steroids in teleosts as well (Das, Khan, & Maitra, ). Both insr and igf1r are also expressed by zebrafish and carp oocytes, and expression of insr is lower than that of igf1r (reviewed by Das et al, ). Zebrafish mid‐vitellogenic follicle‐enclosed oocytes (Figure b) respond to insulin, but not human chorionic gonadotropin, suggesting that oocytes are only responsive to insulin at an early stage of development (Das et al, ).…”

Section: Insulin Regulation Of Oogenesis and Ovarian Developmentmentioning

confidence: 99%

“…Insulin likely triggers meiotic resumption by up‐regulating membrane abundance of Progesterone receptor α and 20β‐hydroxy‐steroid dehydrogenase, which is responsible for maturation‐inducing steroid synthesis (Das et al, ). In vitro insulin stimulation can also trigger igf3 expression in zebrafish follicle‐enclosed oocytes (Das et al, ), suggesting an important role for insulin in modulating the activity of local paracrine factors involved in oocyte maturation (Das et al, ).…”

Section: Insulin Regulation Of Oogenesis and Ovarian Developmentmentioning

confidence: 99%

“…As in mammals, high cAMP/PKA levels maintain prophase-I arrest in lower vertebrates (Das, Khan, & Maitra, 2017). In teleosts, prior to ovulation, a surge in pituitary LH triggers follicle cells to synthesize and secrete maturation-inducing steroid-17α,20β-dihydroxy-4-pregnen-3one in the majority of fishes, but 17α,20β,21-trihydroxy-4-pregnen-3one in sciaenids and in marine perciform species (Nagahama & Yamashita, 2008).…”

Section: Oocyte Growth Development and Maturation In Lower Vertebmentioning

confidence: 99%

“…Binding of maturation‐inducing steroid to its membrane progestin receptor α at the oocyte surface activates a pertussis toxin‐sensitive inhibitory G protein (Gα i ) and subsequently down‐regulates activity of adenylyl cyclase, the enzyme responsible for production of cAMP from adenosine triphosphate (ATP) (Zhu, Rice, Pang, Pace, & Thomas, ). In addition, the maturation‐inducing steroid triggers rapid changes to intracellular phosphorylation–dephosphorylation signaling cascades that ultimately result in the activation of MPF and final oocyte maturation (Das et al, ; Nagahama & Yamashita, ).…”

Section: Insulin Regulation Of Oogenesis and Ovarian Developmentmentioning

confidence: 99%

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Conserved insulin signaling in the regulation of oocyte growth, development, and maturation

2017

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Insulin signaling regulates various aspects of physiology, such as glucose homeostasis and aging, and is a key determinant of female reproduction in metazoans. That insulin signaling is crucial for female reproductive health is clear from clinical data linking hyperinsulinemic and hypoinsulinemic condition with certain types of ovarian dysfunction, such as altered steroidogenesis, polycystic ovary syndrome, and infertility. Thus, understanding the signaling mechanisms that underlie the control of insulin-mediated ovarian development is important for the accurate diagnosis of and intervention for female infertility. Studies of invertebrate and vertebrate model systems have revealed the molecular determinants that transduce insulin signaling as well as which biological processes are regulated by the insulin-signaling pathway. The molecular determinants of the insulin-signaling pathway, from the insulin receptor to its downstream signaling components, are structurally and functionally conserved across evolution, from worms to mammals – yet, physiological differences in signaling still exist. Insulin signaling acts cooperatively with gonadotropins in mammals and lower vertebrates to mediate various aspects of ovarian development, mainly owing to evolution of the endocrine system in vertebrates. In contrast, insulin signaling in Drosophila and Caenorhabditis elegans directly regulates oocyte growth and maturation. In this review, we compare and contrast insulin-mediated regulation of ovarian functions in mammals, lower vertebrates, C. elegans, and Drosophila, and highlight conserved signaling pathways and regulatory mechanisms in general while illustrating insulin’s unique role in specific reproductive processes.

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Inhibition of Oocyte Maturation by Malathion and Structurally Related Chemicals in Zebrafish (Danio rerio) After In Vitro and In Vivo Exposure

Miller

Essen

Brinkmann

et al. 2022

Enviro Toxic and Chemistry

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Oogenesis is the process by which a primary oocyte develops into a fertilizable oocyte, making it critical to successful reproduction in fish. In zebrafish (Danio rerio), there are five stages of oogenesis. During the final step (oocyte maturation), the maturation-inducing hormone 17α,20β-dihydroxy-4-pregnen-3-one (MIH) activates the membrane progestin receptor, inducing germinal vesicle breakdown. Using in vitro assays, it has been shown that anthropogenic stressors can dysregulate MIH-induced oocyte maturation. However, it is unknown whether the in vitro assay is predictive of reproductive performance after in vivo exposure. We demonstrate that a known inhibitor of oocyte maturation, malathion, and a structurally related chemical, dimethoate, inhibit oocyte maturation. However, malaoxon and omethoate, which are metabolites of malathion and dimethoate, did not inhibit oocyte maturation. Malathion and dimethoate inhibited maturation to a similar magnitude when oocytes were exposed for 4 h in vitro or 10 days in vivo, suggesting that the in vitro zebrafish oocyte maturation assay might be predictive of alterations to reproductive performance. However, when adult zebrafish were exposed to malathion for 21 days, there was no alteration in fecundity or fertility in comparison with control fish. Our study supports the oocyte maturation assay as being predictive of the success of in vitro oocyte maturation after in vivo exposure, but it remains unclear whether inhibition of MIH-induced oocyte maturation in vitro correlates to decreases in reproductive performance.

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Endocrine and paracrine regulation of meiotic cell cycle progression in teleost oocytes: cAMP at the centre of complex intra-oocyte signalling events

Cited by 33 publications

References 61 publications

CD38 affects the biological behavior and energy metabolism of nasopharyngeal carcinoma cells

CD38 affects the biological behavior and energy metabolism of nasopharyngeal carcinoma cells

Conserved insulin signaling in the regulation of oocyte growth, development, and maturation

Inhibition of Oocyte Maturation by Malathion and Structurally Related Chemicals in Zebrafish (Danio rerio) After In Vitro and In Vivo Exposure

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