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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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 |
work_keys_str_mv |
AT peltoketoh animalmodelsforaberrationsofgonadotropinaction AT zhangfp animalmodelsforaberrationsofgonadotropinaction AT rullisb animalmodelsforaberrationsofgonadotropinaction |
_version_ |
1782027966031593472 |