Follicle-Stimulating Hormone and Estradiol Interact to Stimulate Glutathione Synthesis in Rat Ovarian Follicles and Granulosa Cells1

Hoang, Yvonne D.; Nakamura, Brooke N.; Luderer, Ulrike

doi:10.1095/biolreprod.109.078378

Cited by 25 publications

(11 citation statements)

References 58 publications

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“…In contrast, mRNA expression for anti-apoptosis factors increased in cultured SAFs compared to in vivo -derived SAFs, including glutamate-cysteine ligase catalytic subunit ( GCLC ) and epidermal growth factor receptor ( EGFR ) (Table 9.1). Exogenous FSH in the culture media may promote the GCLC and EGFR mRNA expression, as reported in rat SAF and granulosa cell culture (Hoang, 2009; Fujinaga, 1994). …”

Section: Comparison Of Gene Expression Between In Vivo- and In Vitro-mentioning

confidence: 54%

Primate Follicular Development and Oocyte Maturation In Vitro

Bernuci

et al. 2013

Advances in Experimental Medicine and Biology

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The factors and processes involved in primate follicular development are complex and not fully understood. An encapsulated three-dimensional (3D) follicle culture system could be a valuable in vitro model to study the dynamics and regulation of folliculogenesis in intact individual follicles in primates. Besides the research relevance, in vitro follicle maturation (IFM) is emerging as a promising approach to offer options for fertility preservation in female patients with cancer. This review summarizes the current published data on in vitro follicular development from the preantral to small antral stage in nonhuman primates, including follicle survival and growth, endocrine (ovarian steroid hormone) and paracrine/autocrine (local factor) function, as well as oocyte maturation and fertilization. Future directions include major challenges and strategies to further improve follicular growth and differentiation with oocytes competent for in vitro fertilization and subsequent embryonic development, as well as opportunities to investigate primate folliculogenesis by utilizing this 3D culture system. The information may be valuable in identifying optimal conditions for human follicle culture, with the ultimate goal of translating the experimental results and products to patients, thereby facilitating diagnostic and therapeutic approaches for female fertility.

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Section: Comparison Of Gene Expression Between In Vivo- and In Vitro-mentioning

confidence: 54%

Primate Follicular Development and Oocyte Maturation In Vitro

Bernuci

et al. 2013

Advances in Experimental Medicine and Biology

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“…Ovarian stimulation with eCG increases protein expression of the modifier (GCLM) and catalytic (GCLC) subunits of glutamate cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis, increasing GCL catalytic activity and GSH concentrations in the rat ovary (Aten et al 1992;Luderer et al 2001;Tsai-Turton and Luderer 2005). Studies in cultured rat antral follicles and granulosa cells show that FSH and estradiol interact to increase mRNA and protein expression of Gclc and Gclm (Tsai-Turton and Luderer 2006;Hoang et al 2009). Deletion of Gclc in mice is embryonic lethal before gestational day 8.5 (Dalton et al 2000;Shi et al 2000).…”

Section: Hormonal Regulation Of and Effects Of Depleting Or Enhancingmentioning

confidence: 99%

Ovarian Toxicity from Reactive Oxygen Species

Luderer¹

2014

Vitamins &Amp; Hormones

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117

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Oxidative stress occurs when cellular mechanisms to regulate levels of reactive oxygen species (ROS) are overwhelmed due to overproduction of ROS and/or deficiency of antioxidants. This chapter describes accumulating evidence that oxidative stress is involved in ovarian toxicity caused by diverse stimuli, including environmental toxicants. There is strong evidence that ROS are involved in initiation of apoptosis in antral follicles caused by several chemical and physical agents. Although less attention has been focused on the roles of ROS in primordial and primary follicle death, several studies have shown protective effects of antioxidants and/or evidence of oxidative damage, suggesting that ROS may play a role in these smaller follicles as well. Oxidative damage to lipids in the oocyte has been implicated as a cause of persistently poor oocyte quality after early life exposure to several toxicants. Developing germ cells in the fetal ovary have also been shown to be sensitive to toxicants and ionizing radiation, which induce oxidative stress. Recent studies have begun to elucidate the mechanisms by which ROS mediate ovarian toxicity.

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“…Effect of GSH on progesterone production and the viability of preovulatory GCs in response to arsenite treatment FSH plays an anti-apoptotic effect by enhancing GSH synthesis in preovulatory follicles (Luderer et al, 2001;Tsai-Turton and Luderer, 2006;Hoang et al, 2009). In addition, GSH is involved in Leydig cell steroidogenesis (Diemer et al, 2003;Chen et al, 2008).…”

Section: Activation Of Caspase-3 Regulates Progesterone Production Inmentioning

confidence: 99%

Arsenic induced progesterone production in a caspase‐3‐dependent manner and changed redox status in preovulatory granulosa cells

Yuan

Yao

et al. 2011

Journal Cellular Physiology

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Arsenic contamination is a principal environmental health threat throughout the world. However, little is known about the effect of arsenic on steroidogenesis in granulosa cells (GCs). We found that the treatment of preovulatory GCs with arsenite stimulated progesterone production. A significant increase in serum level of progesterone was observed in female Sprague-Dawley rats following arsenite treatment at a dose of 10 mg/L/rat/day for 7 days. Further experiments demonstrated that arsenite treatment did not change the level of intracellular cyclic AMP (cAMP) or phosphorylated ERK1/2 in preovulatory GCs; however, progesterone production was significantly decreased when cAMP-dependent protein kinase (PKA) or ERK1/2 pathway was inhibited. This implied that the effect of arsenite on progesterone production may require cAMP/PKA and ERK1/2 signaling but not depend on them. Furthermore, we found that arsenite decreased intracellular reactive oxygen species (ROS) but increased the antioxidant glutathione (GSH) levels and mitochondrial membrane potential (ΔΨm) in parallel to the changes in progesterone production. Progesterone antagonist blocked the arsenic-stimulated increase of GSH levels. Arsenite treatment induced caspase-3 activation, although no apoptosis was observed. Inhibition of caspase-3 activity significantly decreased progesterone production stimulated by arsenite or follicle-stimulating hormone (FSH). GSH depletion with buthionine sulfoximine led to cell apoptosis in response to arsenite treatment. Collectively, this study demonstrated for the first time that arsenite stimulates progesterone production through cleaved/active caspase-3-dependent pathway, and the increase of GSH level promoted by progesterone production may protect GCs against apoptosis and maintain the steroidogenesis of GCs in response to arsenite treatment.

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Follicle-Stimulating Hormone and Estradiol Interact to Stimulate Glutathione Synthesis in Rat Ovarian Follicles and Granulosa Cells1

Cited by 25 publications

References 58 publications

Primate Follicular Development and Oocyte Maturation In Vitro

Primate Follicular Development and Oocyte Maturation In Vitro

Ovarian Toxicity from Reactive Oxygen Species

Arsenic induced progesterone production in a caspase‐3‐dependent manner and changed redox status in preovulatory granulosa cells

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