Literature DB >> 19059463

Role of androgen and gonadotrophins in the development and function of the Sertoli cells and Leydig cells: data from mutant and genetically modified mice.

P J O'Shaughnessy1, I D Morris, I Huhtaniemi, P J Baker, M H Abel.   

Abstract

Development and maintenance of the male phenotype and establishment of fertility are all dependent upon the activity of the Sertoli cells and Leydig cells of the testis. This review examines the regulation and function of these cell during fetal and post-natal development. Fetal Leydig cells are sensitive to both luteinising hormone (LH) and adrenocorticotrophic hormone (ACTH) but Leydig cell function appears normal in fetal mice lacking both hormones or their receptors. Post-natally, the Sertoli cells and Leydig cells are reliant upon the pituitary gonadotrophins. Leydig cells are critically dependent on LH but follicle-stimulating hormone (FSH), presumably acting through the Sertoli cell, can also affect Leydig cell function. Testosterone secreted by the Leydig cells acts with FSH to stimulate Sertoli cell activity and spermatogenesis. Study of animals lacking FSH-receptors and androgen-receptors shows that both hormones can act to maintain the meiotic germ cell population but that androgens are critical for completion of meiosis.

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Year:  2008        PMID: 19059463     DOI: 10.1016/j.mce.2008.11.005

Source DB:  PubMed          Journal:  Mol Cell Endocrinol        ISSN: 0303-7207            Impact factor:   4.102


  24 in total

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Authors:  Cathryn A Hogarth; Michael D Griswold
Journal:  J Clin Invest       Date:  2010-04-01       Impact factor: 14.808

Review 2.  Endocrine control of spermatogenesis: Role of FSH and LH/ testosterone.

Authors:  Suresh Ramaswamy; Gerhard F Weinbauer
Journal:  Spermatogenesis       Date:  2015-01-26

3.  Isolation of Sertoli, Leydig, and spermatogenic cells from the mouse testis.

Authors:  Yao-Fu Chang; Jennifer S Lee-Chang; Subbarayalu Panneerdoss; James A MacLean; Manjeet K Rao
Journal:  Biotechniques       Date:  2011-11       Impact factor: 1.993

4.  Sexually dimorphic testosterone secretion in prenatal and neonatal mice is independent of kisspeptin-Kiss1r and GnRH signaling.

Authors:  Matthew C Poling; Alexander S Kauffman
Journal:  Endocrinology       Date:  2011-12-27       Impact factor: 4.736

5.  Rex1 (Zfp42) null mice show impaired testicular function, abnormal testis morphology, and aberrant gene expression.

Authors:  Naira C Rezende; Mi-Young Lee; Sébastien Monette; Willie Mark; Ailan Lu; Lorraine J Gudas
Journal:  Dev Biol       Date:  2011-05-27       Impact factor: 3.582

6.  The Leydig cell MEK/ERK pathway is critical for maintaining a functional population of adult Leydig cells and for fertility.

Authors:  Soichi Yamashita; Ping Tai; Jean Charron; CheMyong Ko; Mario Ascoli
Journal:  Mol Endocrinol       Date:  2011-04-28

7.  The ERK1/2 pathway regulates testosterone synthesis by coordinately regulating the expression of steroidogenic genes in Leydig cells.

Authors:  Maria Eugenia Matzkin; Soichi Yamashita; Mario Ascoli
Journal:  Mol Cell Endocrinol       Date:  2013-03-07       Impact factor: 4.102

8.  AKAP9 is essential for spermatogenesis and sertoli cell maturation in mice.

Authors:  Kerry J Schimenti; Sky K Feuer; Laurie B Griffin; Nancy R Graham; Claire A Bovet; Suzanne Hartford; Janice Pendola; Carl Lessard; John C Schimenti; Jeremy O Ward
Journal:  Genetics       Date:  2013-04-22       Impact factor: 4.562

Review 9.  Hypothalamic control of the male neonatal testosterone surge.

Authors:  Jenny Clarkson; Allan E Herbison
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2016-02-01       Impact factor: 6.237

10.  Transcriptional profiling of luteinizing hormone receptor-deficient mice before and after testosterone treatment provides insight into the hormonal control of postnatal testicular development and Leydig cell differentiation.

Authors:  D K Griffin; P J Ellis; B Dunmore; J Bauer; M H Abel; N A Affara
Journal:  Biol Reprod       Date:  2010-02-17       Impact factor: 4.285

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