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Chapter 26 - Male Contraception
- from Section 4 - Treatment of Male Infertility
- Edited by Larry I. Lipshultz, Baylor College of Medicine, Texas, Stuart S. Howards, University of Virginia, Craig S. Niederberger, University of Illinois, Chicago, Dolores J. Lamb, Weill Cornell Medical College, New York
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- Book:
- Infertility in the Male
- Published online:
- 08 July 2023
- Print publication:
- 15 June 2023, pp 477-494
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Summary
Contraception, or the purposeful temporary inhibition of one’s own fertility, is a vital additional level of control over family planning. Though many potent and reversible contraceptives are on the market, most of these contraceptives are for women – leaving a disproportionate burden of the responsibility for contraception and family planning on women. Reversible forms of contraception available for men are limited to the use of condoms and withdrawal. The only other form of male contraception that approaches the same efficacy as some available options for women is vasectomy, which is not always reversible and often has lasting effects on fertility [1]. To meet the unmet need of potent and reversible male contraception, research and clinical trials for hormonal male contraceptives have been ongoing for nearly the past 50 years; yet roadblocks, such as unfavorable injections and undesirable side effects, have slowed the emergence of this option on the market [2, 3]. New research is now under way for optimized hormonal contraceptives and a myriad of nonhormonal contraceptive options. Early preclinical tests of nonhormonal contraceptive compounds in animal models and in small clinical studies have successfully demonstrated that pharmacological compounds targeting specific proteins can result in complete and reversible contraceptive efficacy. However, since many compounds used in early studies were not specifically tailored for their use as contraceptives in some cases, or due to the potential for off-target effects identified from preclinical testing, more work is needed to improve these compounds for selectivity and to identify novel protein targets [4–6]. Nonetheless, the plethora of research and clinical advances made in this field in recent years has done much to make a male contraceptive pill closer to reality. In this chapter, we discuss the history and recent advances in novel hormonal and nonhormonal contraceptive development and provide a brief overview of how contraceptive compounds modulate the dynamics of sperm production and transport.
7 - Mouse models to identify genes throughout oogenesis
- from Section 2 - Life cycle
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- By Jia Peng, Departments of Molecular and Human Genetics, and Pathology and Immunology, Baylor College of Medicine, Houston, TX, USA, Qinglei Li, Department of Veterinary Integrative Biosciences, Texas A and M University, College Station, TX, USA, Martin M. Matzuk, Departments of Molecular and Human Genetics, Pathology and Immunology, Molecular and Cellular Biology, and Pharmacology, Baylor College of Medicine, Houston, TX, USA
- Edited by Alan Trounson, Roger Gosden, Ursula Eichenlaub-Ritter, Universität Bielefeld, Germany
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- Book:
- Biology and Pathology of the Oocyte
- Published online:
- 05 October 2013
- Print publication:
- 24 October 2013, pp 73-80
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Summary
Introduction
In mammals, oocytes initially develop from primordial germ cells (PGCs), which divide and migrate to the gonad to become oogonia during fetal development. At birth, a mammalian female contains about two million primary oocytes, which remain quiescent in the prophase of meiosis I (refer to Chapters 2 and 6). Eventually, a subset of these immature oocytes will be surrounded by granulosa cells to form the primordial follicle pool. Folliculogenesis begins with the activation of a primordial follicle and ends with either the release of a fertilizable oocyte or follicular atresia. The pathways involved in oogenesis and folliculogenesis have been extensively studied, with an attempt to better understand the molecular mechanisms underlying successful ovulation and fertilization. In this chapter, we highlight three major pathways critical for female germ cell development – transforming growth factor beta (TGFβ), phosphatidylinositol 3-kinase (PI3K), and small RNAs – and discuss mouse models used for dissecting the function of genes involved in these pathways.
Overview of the TGFβ pathway
The TGFβ superfamily is the largest family of secreted proteins in mammals [1]. Members of the TGFβ family are involved in a variety of developmental and physiological processes. The canonical TGFβ signaling pathway begins with two dimeric ligands binding to type I and type II receptors to form an activated heterotetrameric receptor complex. The type II receptor within this activated complex phosphorylates the type I receptor, which in turn phosphorylates downstream SMAD proteins. These phosphorylated, receptor-regulated SMAD (R-SMAD) proteins can then bind to the common SMAD (co-SMAD; i.e., SMAD4), translocate into the nucleus, and interact with SMAD binding partners to regulate transcription of target genes (Figure 7.1).
Local signalling environments and human male infertility: what we can learn from mouse models
- Roopa L. Nalam, Martin M. Matzuk
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- Journal:
- Expert Reviews in Molecular Medicine / Volume 12 / January 2010
- Published online by Cambridge University Press:
- 11 May 2010, e15
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- Article
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Infertility is one of the most prevalent public health problems facing young adult males in today's society. A clear, treatable cause of infertility cannot be determined in a large number of these patients, and a growing body of evidence suggests that infertility in many of these men may be due to genetic causes. Studies using mouse knockout technology have been integral for examination of normal spermatogenesis and to identify proteins essential for this process, which in turn are candidate genes for human male infertility. Successful spermatogenesis depends on a delicate balance of local signalling factors, and this review focuses on the genes that encode these factors. Normal functioning of all testicular cell types is essential for fertility and might also be crucial to prevent germ cell oncogenesis. Analysis of these signalling processes in spermatogenesis using mouse models has provided investigators with an invaluable tool to effectively translate basic science research to the research of human disease and infertility.