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Professor Cheng Peng from Sun Yat-sen University published new results in stem cell research
In a groundbreaking study, researchers from Sun Yat-sen University have uncovered the unique properties of testicular Leydig stem cells (SLCs), highlighting their potential as a promising cell source for treating testosterone deficiency in men. The findings were recently published in the journal *Cell Research*, marking an important step forward in male hormone therapy.
The lead author of the study is Professor Andy Peng Xiang from Zhongshan Medical College at Sun Yat-sen University. A renowned expert in stem cell biology and developmental genetics, he has made significant contributions to gene knockout and transgenic animal research. To date, he has authored over 30 scientific papers, establishing himself as a key figure in the field.
Testosterone plays a critical role in male physiology, influencing everything from fetal development to aging. It's essential for gender differentiation, growth, and overall bodily function, and also impacts mood, behavior, and mental health. Testosterone deficiency is a common condition among men of all ages, leading to issues like fatigue, sexual dysfunction, and cognitive decline. While Leydig cell (LC) transplantation has shown promise, it faces challenges due to the limited lifespan and inability of mature LCs to proliferate effectively.
Leydig cells are responsible for testosterone production in the testes, crucial for secondary sexual characteristics and sperm development. According to recent data, over 4.5 million men in the U.S. experience symptoms linked to low testosterone. However, traditional LC transplants often fail due to poor long-term functionality.
SLCs, the precursor cells to LCs, offer a more sustainable solution. These cells can self-renew and produce testosterone, making them ideal for therapeutic applications. However, isolating SLCs has been difficult due to the lack of specific markers.
In this new study, the team used flow cytometry and functional assays to identify SLCs based on Nestin (Nes) expression. In a mouse model where Nes drives GFP, they found that Nes-GFP+ cells localized in the interstitial space, expressing LIFR and PDGFR-α—markers not typically associated with LCs. These cells demonstrated clonogenic potential, self-renewal, and the ability to differentiate into multiple lineages, including LCs, while producing testosterone.
When transplanted into models with damaged or aged Leydig cells, the Nes-GFP+ cells successfully restored testosterone levels, promoting meiosis and germ cell recovery. The researchers also identified CD51 as a potential surface marker for SLCs, expanding the tools available for future research and treatment strategies.
This discovery could revolutionize the treatment of testosterone deficiency, offering a more effective and lasting solution for men suffering from hormonal imbalances.