Animal models for aberrations of gonadotropin action

During the last two decades a large number of genetically modified mouse lines with altered gonadotropin action have been generated. These mouse lines fall into three categories: the lack-of-function mice, gain-of-function mice, and the mice generated by breeding the abovementioned lines with other...

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Autores principales: Peltoketo, H., Zhang, F.-P., Rulli, S.B.
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_13899155_v12_n4_p245_Peltoketo
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spelling todo:paper_13899155_v12_n4_p245_Peltoketo2023-10-03T16:12:48Z Animal models for aberrations of gonadotropin action Peltoketo, H. Zhang, F.-P. Rulli, S.B. Gonadotropin Ovary. Testis Pituitary. Genetically modified Receptor chorionic gonadotropin follitropin gonadotropin hypophysis hormone luteinizing hormone article carcinogenesis disease model genetic disorder hypergonadotropic hypogonadism hypogonadotropic hypogonadism hypophysis hypothalamus hypophysis gonad system male accessory gland nonhuman ovary ovary follicle phenotype testis urogenital system Animals Disease Models, Animal Endocrine System Diseases Female Gonadotropins Humans Male Mice Mice, Transgenic Ovary Pituitary Gland Testis During the last two decades a large number of genetically modified mouse lines with altered gonadotropin action have been generated. These mouse lines fall into three categories: the lack-of-function mice, gain-of-function mice, and the mice generated by breeding the abovementioned lines with other disease model lines. The mouse strains lacking gonadotropin action have elucidated the necessity of the pituitary hormones in pubertal development and function of gonads, and revealed the processes from the original genetic defect to the pathological phenotype such as hypo- or hypergonadotropic hypogonadism. Conversely, the strains of the second group depict consequences of chronic gonadotropin action. The lines vary from those expressing constitutively active receptors and those secreting follicle-stimulating hormone (FSH) with slowly increasing amounts to those producing human choriogonadotropin (hCG), amount of which corresponds to 2000-fold luteinizing hormone (LH)/hCG biological activity. Accordingly, the phenotypes diverge from mild anomalies and enhanced fertility to disrupted gametogenesis, but eventually chronic, enhanced and non-pulsatile action of both FSH and LH leads to female and male infertility and/or hyper- and neoplasias in most of the gonadotropin gain-offunction mice. Elevated gonadotropin levels also alter the function of several extra-gonadal tissues either directly or indirectly via increased sex steroid production. These effects include promotion of tumorigenesis in tissues such as the pituitary, mammary and adrenal glands. Finally, the crossbreedings of the current mouse strains with other disease models are likely to uncover the contribution of gonadotropins in novel biological systems, as exemplified by the recent crossbreed of LHCG receptor deficient mice with Alzheimer disease mice. © Springer Science+Business Media, LLC 2011. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_13899155_v12_n4_p245_Peltoketo
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Gonadotropin
Ovary. Testis
Pituitary. Genetically modified
Receptor
chorionic gonadotropin
follitropin
gonadotropin
hypophysis hormone
luteinizing hormone
article
carcinogenesis
disease model
genetic disorder
hypergonadotropic hypogonadism
hypogonadotropic hypogonadism
hypophysis
hypothalamus hypophysis gonad system
male accessory gland
nonhuman
ovary
ovary follicle
phenotype
testis
urogenital system
Animals
Disease Models, Animal
Endocrine System Diseases
Female
Gonadotropins
Humans
Male
Mice
Mice, Transgenic
Ovary
Pituitary Gland
Testis
spellingShingle Gonadotropin
Ovary. Testis
Pituitary. Genetically modified
Receptor
chorionic gonadotropin
follitropin
gonadotropin
hypophysis hormone
luteinizing hormone
article
carcinogenesis
disease model
genetic disorder
hypergonadotropic hypogonadism
hypogonadotropic hypogonadism
hypophysis
hypothalamus hypophysis gonad system
male accessory gland
nonhuman
ovary
ovary follicle
phenotype
testis
urogenital system
Animals
Disease Models, Animal
Endocrine System Diseases
Female
Gonadotropins
Humans
Male
Mice
Mice, Transgenic
Ovary
Pituitary Gland
Testis
Peltoketo, H.
Zhang, F.-P.
Rulli, S.B.
Animal models for aberrations of gonadotropin action
topic_facet Gonadotropin
Ovary. Testis
Pituitary. Genetically modified
Receptor
chorionic gonadotropin
follitropin
gonadotropin
hypophysis hormone
luteinizing hormone
article
carcinogenesis
disease model
genetic disorder
hypergonadotropic hypogonadism
hypogonadotropic hypogonadism
hypophysis
hypothalamus hypophysis gonad system
male accessory gland
nonhuman
ovary
ovary follicle
phenotype
testis
urogenital system
Animals
Disease Models, Animal
Endocrine System Diseases
Female
Gonadotropins
Humans
Male
Mice
Mice, Transgenic
Ovary
Pituitary Gland
Testis
description During the last two decades a large number of genetically modified mouse lines with altered gonadotropin action have been generated. These mouse lines fall into three categories: the lack-of-function mice, gain-of-function mice, and the mice generated by breeding the abovementioned lines with other disease model lines. The mouse strains lacking gonadotropin action have elucidated the necessity of the pituitary hormones in pubertal development and function of gonads, and revealed the processes from the original genetic defect to the pathological phenotype such as hypo- or hypergonadotropic hypogonadism. Conversely, the strains of the second group depict consequences of chronic gonadotropin action. The lines vary from those expressing constitutively active receptors and those secreting follicle-stimulating hormone (FSH) with slowly increasing amounts to those producing human choriogonadotropin (hCG), amount of which corresponds to 2000-fold luteinizing hormone (LH)/hCG biological activity. Accordingly, the phenotypes diverge from mild anomalies and enhanced fertility to disrupted gametogenesis, but eventually chronic, enhanced and non-pulsatile action of both FSH and LH leads to female and male infertility and/or hyper- and neoplasias in most of the gonadotropin gain-offunction mice. Elevated gonadotropin levels also alter the function of several extra-gonadal tissues either directly or indirectly via increased sex steroid production. These effects include promotion of tumorigenesis in tissues such as the pituitary, mammary and adrenal glands. Finally, the crossbreedings of the current mouse strains with other disease models are likely to uncover the contribution of gonadotropins in novel biological systems, as exemplified by the recent crossbreed of LHCG receptor deficient mice with Alzheimer disease mice. © Springer Science+Business Media, LLC 2011.
format JOUR
author Peltoketo, H.
Zhang, F.-P.
Rulli, S.B.
author_facet Peltoketo, H.
Zhang, F.-P.
Rulli, S.B.
author_sort Peltoketo, H.
title Animal models for aberrations of gonadotropin action
title_short Animal models for aberrations of gonadotropin action
title_full Animal models for aberrations of gonadotropin action
title_fullStr Animal models for aberrations of gonadotropin action
title_full_unstemmed Animal models for aberrations of gonadotropin action
title_sort animal models for aberrations of gonadotropin action
url http://hdl.handle.net/20.500.12110/paper_13899155_v12_n4_p245_Peltoketo
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