Engraftment of Three Types of Stem Leyding Cells (CD51+, p75-positive and Nestin-positive): A Treatment Strategy for Testosterone Deficiency and Testicular Leyding Cell Dysfunction
Engraftment of Three Types of Stem Leyding Cells (CD51+, p75-positive and Nestin-positive): A Treatment Strategy for Testosterone Deficiency and Testicular Leyding Cell Dysfunction
Introduction: Testosterone is produced by stem leyding cells (SLCs), which reside in the testis interstitium. Testosterone deficiency (TD) is a public health concern which is characterized by various symptoms such as sexual dysfunction and osteoporosis. Since SLC replacement therapy has provided a long-lasting system for testosterone delivery, in this article I will review the engraftment of what types of SLCs have effect on TD.
Methods: This review article has been extracted from 5 article that has indexed in PubMed and Google Scholar and published from year 2014 to 2022. The search terms include “Stem Leyding Cell”, “CD51”, “Nestin”, “p75-positive”, “Testosterone” and “Transplantation”.
Results: p75 neurotrophin receptor positive (p75⁺) cells demonstrated clonogenic self-renewal capacity and had differentiation potential into testosterone producing Leyding cells (LCs) in vitro and in vivo. GFP driven by the Nestin (Nes) promoter which have been identified as Nes-GFP⁺ had the ability to extensive proliferation in vitro and when these cells grafted onto testes of LC-disrupted rat models, the Nes-GFP⁺ cells produced testosterone. And these results are similar to the transplantation of CD51⁺ SLCs that were successful in differentiating into mature LCs, and secretion of testosterone.
Conclusion: Transplantation of three types of SLCs, which are p75⁺, Nes-GFP⁺ and CD51⁺ may influence TD and testicular leyding cell dysfunction by improving serum testosterone levels, meiotic and post-meiotic germ cell recovery and spermatogenesis which all of these influences might be regulated by the hypothalamic-pituitary-gonadal (HPG) axis. However, further studies are required to confirm the positive impact of p75⁺, Nes-GFP⁺ and CD51⁺ transplantation on TD.