Male Germ Cell Development in Humans

Abstract

Background: Germ cells are unique cells that possess the ability to transmit genetic information between generations. Detailed knowledge about the molecular and cellular mechanisms determining the fate of human male germ cells still remains sparse. This is partially due to ethical issues limiting the access to research material. Therefore, the mechanisms of proliferation, differentiation and apoptosis of human male germ cells still remain challenging study objectives. Methods: This review focuses on using English articles accessible in PubMed as well as personal files on the current knowledge of the molecular and cellular mechanisms connected with human testicular germ cell development, maturation failure and the possibility of fertility preservation in patients in whom there is a risk of gonadal failure. However, since rodents, particularly mice, offer the possibility of studying germ cell development by use of genetic modification techniques, some studies using animal models are also discussed. Conclusion: This mini review focuses on the current knowledge about male germ cells. However, the reader is referred to two previous mini reviews focusing on testicular somatic cells, i.e. on Sertoli cells and Leydig cells.

Testicular function and fertility preservation after treatment for haematological cancer

“…These spermatogonia may theoretically be differentiated ex vivo into mature sperms. The main models for ex-vivo differentiation of male germ cells include in-vitro culture systems; testicular tissue (xeno)grafting and SSC transplantation into the seminiferous tubules of the testis [33][34][35]. All of these options for germ cell differentiation into functional sperm in various animal models require a functional somatic microenvironment (or 'niche') similar to that of the healthy testis in vivo.…”

Development and Disease-Dependent Dynamics of Spermatogonial Subpopulations in Human Testicular Tissues

“…For comparable results, spermatogonial density (numbers per mm 3 ; N nuc,testis ) were determined using a previously published equation [46].…”

“…Impairment of spermatogonial development before or during puberty may lead to infertility in adult life. Reasons for this include pathological conditions such as cryptorchidism and genetic or endocrine disorders [1][2][3][4][5]. Apart from that, cancer therapy and conditioning treatments of non-malignant diseases such as sickle cell disease and thalassemia, are known to induce testicular damage, affect spermatogonial function and reduce or even deplete germ cells [4][5][6][7][8][9][10].…”

No evidence for mosaic pathogenic copy number variations in cardiac tissue from patients with congenital heart malformations

“…In utero, PGCs entering testis migrate to the basal membrane of the primitive sex cords where they rest until after birth, surrounded by supportive Sertoli cells that provide nutrients and a protective environment. Around six months after birth they differentiate into spermatogonia (3). Spermatogenesis starts in early puberty when the sex cords acquire a lumen and develop into the seminiferous tubules of the testis.…”