Ovarian localization of 11β-hydroxysteroid dehydrogenase (11βHSD): effects of ACTH stimulation and its relationship with bovine cystic ovarian disease

Amweg, Ayelén Noelia; Salvetti, Natalia Raquel; Stangaferro, M.L.; Paredes, Alfonso; Lara, Hernán; Rodríguez, Fernanda Mariel; Ortega, Hugo Héctor

doi:10.1016/j.domaniend.2013.07.001

Cited by 42 publications

(95 citation statements)

References 77 publications

(123 reference statements)

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“…Although it has not been demonstrated that the ovary is able to produce GCs de novo, we have demonstrated that ACTH is able to stimulate the secretion of cortisol in the follicular wall in culture [Amweg et al, 2011], induce steroid hormone secretion and produce changes in 11β-hydroxysteroid dehydrogenase expression by the ovary [Amweg et al, 2013], indicating that ACTH may be involved in regulatory mechanisms related to ovarian function associated with ovulation, ovarian steroidogenesis, luteal function and COD pathogenesis [Tetsuka, 2007;Amweg et al, 2011Amweg et al, , 2013.…”

Section: Introductionmentioning

confidence: 56%

“…The model of ACTH-induced ovarian follicular cysts used in the present study has been previously described in detail [Dobson et al, 2000;Ortega et al, 2008;Salvetti et al, 2010Salvetti et al, , 2012Amweg et al, 2013]. Briefly, beginning on day 15 of a synchronized estrous cycle, 5 heifers received subcutaneous injections of 1 mg of a syn-140 thetic polypeptide with ACTH activity (Synacthen Depot; Novartis, Basel, Switzerland) every 12 h for 7 days (treated group), whereas the other 5 animals received saline solution (1 ml; control group).…”

Section: Induction Of Cod By Acth Administrationmentioning

confidence: 99%

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Role of Glucocorticoids in Cystic Ovarian Disease: Expression of Glucocorticoid Receptor in the Bovine Ovary

Amweg

Rodríguez

Huber³

et al. 2015

Cells Tissues Organs

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The aim of this study was to characterize the expression of glucocorticoid receptor (GR) in the components of normal bovine ovary and in animals with cystic ovarian disease (COD). Changes in the protein and mRNA expression levels were determined in control cows and cows with COD by immunohistochemistry and real-time PCR. GR protein expression in granulosa cells was higher in cysts from animals with spontaneous COD and adrenocorticotropic hormone-induced COD than in tertiary follicles from control animals. In theca interna cells, GR expression was higher in cysts from animals with spontaneous COD than in tertiary follicles from control animals. The increase in GR expression observed in cystic follicles suggests a mechanism of action for cortisol and its receptor through the activation/inactivation of specific transcription factors. These factors could be related to the pathogenesis of COD in cattle.

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Section: Introductionmentioning

confidence: 56%

Section: Induction Of Cod By Acth Administrationmentioning

confidence: 99%

Role of Glucocorticoids in Cystic Ovarian Disease: Expression of Glucocorticoid Receptor in the Bovine Ovary

Amweg

Rodríguez

Huber³

et al. 2015

Cells Tissues Organs

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“…The presence of these HSD11Bs in the ovary has been reported in various species such as humans (Michael et al 1993, Albiston et al 1994, Michael et al 1997, Tetsuka et al 1997, Ricketts et al 1998, Smith et al 2000, Rae et al 2004, macaques (Fru et al 2006), cattle (Tetsuka et al 2003, Komiyama et al 2008, Tetsuka et al 2010, Amweg et al 2013, pigs (Sunak et al 2007, Webb et al 2008 and rats (Benediktsson et al 1992, Tetsuka et al 1999b, Gomez-Sanchez et al 2009.…”

Section: Discussionmentioning

confidence: 92%

Glucocorticoid metabolism in the bovine cumulus–oocyte complex matured in vitro

et al. 2016

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Glucocorticoid action in target organs is regulated by relative activities of 11b-HSD type 1 (HSD11B1) that mainly converts cortisone to active cortisol and type 2 (HSD11B2) that inactivates cortisol to cortisone. HSD11Bs have been shown to be expressed in the ovary of various species. However, little is known about the expression and activity of HSD11Bs in the bovine cumulus-oocyte complex (COC). In the present study, we investigated the expression and activities of HSD11Bs in in vitro-matured (IVM) bovine COCs. Bovine COCs were matured in M199 supplemented with or without FSH and FCS. The expression of HSD11B1 and HSD11B2 was measured by using quantitative RT-PCR in denuded oocytes (DO) and cumulus cells (CC). Reductive and oxidative activities of HSD11Bs were determined by radiometric conversion assay using labeled cortisol, cortisone or dexamethasone in intact COCs, DO or CC in the presence or absence of 11-keto-progesterone (11kP), a selective inhibitor of HSD11B2. The presence of HSD11Bs in the oocyte was examined by immunofluorescence microscopy. Oocytes exclusively expressed HSD11B2 and its expression and activity were largely unchanged during IVM. CC, on the other hand, exclusively expressed HSD11B1 and its expression and activity were upregulated as IVM progressed. As a result, the net glucocorticoid metabolism shifted from inactivation to activation towards the end of IVM. These results indicate that the bovine COC is capable of modulating local glucocorticoid concentration and, by doing so, may create an environment that is favorable to ovulating oocyte for maturation, fertilization and subsequent development.

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“…Sin embargo, otros autores postulan que la actividad de este receptor es dependiente del ligando, el IGF se une, produce un cambio conformacional provocando su activación (Kavran et al, 2014). Así, los altos niveles de IGFR1 en quistes podrían estar estimulados por los niveles de 17 β-estradiol tendientes a aumentar en estas estructuras (Amweg et al, 2013), cuando las concentraciones de IGF1 son bajas como ha sido demostrado previamente en quistes (Ortega et al, 2008). De esta manera, el aumento de la expresión del receptor se debería a la necesidad de incrementar la posibilidad de respuesta frente a los bajos niveles de IGF1 detectados en quistes (Ortega et al, 2008;Rodríguez et al, 2015).…”

Section: Expresión De Los Diferentes Componentes Del Sistema Igf En Lunclassified

“…De esta manera, el aumento de la expresión del receptor se debería a la necesidad de incrementar la posibilidad de respuesta frente a los bajos niveles de IGF1 detectados en quistes (Ortega et al, 2008;Rodríguez et al, 2015). Así, los quistes serían capaces de mantener las respuestas a IGF1, tales como la proliferación y la esteroidogénesis activas (Ortega et al, 2008;Amweg et al, 2013).…”

Section: Expresión De Los Diferentes Componentes Del Sistema Igf En Lunclassified

Participación del sistema IGF en la patogenia de la enfermedad quística bovina

Rodríguez¹,

Salvetti²,

Ortega³

et al. 2016

FAVE Cs Vet

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La enfermedad quística ovárica (COD) es una de las principales causas de falla reproductiva y de infertilidad, y constituye uno de los de los trastornos reproductivos más frecuentes en vacas lecheras de alta producción. El desarrollo de esta enfermedad está asociado a un desequilibrio en el eje hipotalámico-hipofisario-gonadal en el cual factores endocrinos, entre ellos el sistema de factores de crecimiento análogos a insulina (IGF), participan en el desarrollo folicular, diferenciación celular y la secreción de hormonas ováricas. Considerando al sistema IGF como un importante regulador del crecimiento y funcionalidad folicular, evaluamos la participación de componentes del sistema IGF en el desarrollo de la COD. Las alteraciones en diferentes componentes del sistema IGF que podrían afectar al normal funcionamiento del ovario participando en el desarrollo de la COD en bovinos.

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Ovarian localization of 11β-hydroxysteroid dehydrogenase (11βHSD): effects of ACTH stimulation and its relationship with bovine cystic ovarian disease

Cited by 42 publications

References 77 publications

Role of Glucocorticoids in Cystic Ovarian Disease: Expression of Glucocorticoid Receptor in the Bovine Ovary

Role of Glucocorticoids in Cystic Ovarian Disease: Expression of Glucocorticoid Receptor in the Bovine Ovary

Glucocorticoid metabolism in the bovine cumulus–oocyte complex matured in vitro

Participación del sistema IGF en la patogenia de la enfermedad quística bovina

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