Recent research on cellular processes in hair loss has revealed important insights into the role of ancient genetic elements known as retrotransposons. These elements, remnants of ancient viral infections and mobile genes, are critical in the development and tissue regeneration of mammals, including humans.
Yejing Ge, an assistant professor at The University of Texas MD Anderson Cancer Center, explains that retrotransposons make up approximately 40% of the mammalian genome. While most retrotransposons have lost the ability to “jump” or move around the genome over millions of years of evolution, many have become indispensable for normal biological functions. However, a rare group of these elements, called endogenous retroviruses (ERVs), can still “jump”—and their uncontrolled movement can cause genetic diseases.
“These evolutionarily young retrotransposons are linked to a range of human health issues, including cancer, autoimmune disorders, and neurodegenerative diseases,” says Ge. “Our bodies have evolved mechanisms to repress their activity, but when these systems fail, the results can be damaging.”
Ge’s team focused on the role of ERVs in hair loss by studying mouse skin stem cells. The research could pave the way for new treatments for hair loss, while also offering fresh insights into the cellular origins of aging and disease.
DNA Methylation and Its Role in Retrotransposon Activity
In early mammalian development, ERVs are typically silenced through DNA methylation—a process where chemical groups are added to DNA to inhibit certain genes. However, the discovery in 1981 by molecular biologist Harold Weintraub and his colleagues revealed that the removal of these methyl groups could reactivate ERVs.
Building on this, Ge and her team investigated the role of SETDB1, an enzyme that mediates the methylation of histones—proteins that help regulate gene activity. When they deleted the SETDB1 gene, ERVs became reactivated. This disruption led to the production of viral-like particles during hair-follicle regeneration, contributing to inflammation and DNA-replication stress, both of which are toxic to cells.
“When SETDB1, a critical repressor, is defective, ERV activity is unleashed, and this can lead to significant cellular damage and hair loss,” Ge explains.
Potential for New Treatments
Remarkably, Ge’s team discovered that by using retroviral drugs to treat the stem cells with reactivated ERVs, they were able to reverse the damage. The treated cells recovered and began generating hair, suggesting that antiviral treatments could hold promise for new approaches to hair loss.
Beyond potential treatments for hair loss, Ge notes that understanding the ongoing “arms race” between retrotransposons and the body’s repressive mechanisms could offer valuable insights into broader health issues. “The maladaptive behavior of stem cells carrying active retrotransposons may contribute to cancer malignancy or the aging process,” she says.
This groundbreaking work not only sheds light on the cellular mechanisms of hair loss but also holds promise for advancing our understanding of human physiology and pathology, potentially leading to novel treatments for a variety of diseases.
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