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Molecule Produced After Skin Injury is Shown to Accelerate Hair Growth

Photo shows the top of a bald man's head.
Photo shows the top of a bald man's head.

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Sarah Avery
Sarah Avery
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DURHAM, N.C. – A molecule that skin tissue produces after injury appears to accelerate hair growth, suggesting a potential new target to reverse hair loss, researchers at Duke University School of Medicine report.

In a study appearing online Feb. 24 in the journal Stem Cell Reports, the researchers describe a unique role for a molecule called thymic stromal lymphopoietin (TSLP). They found TSLP plays a key role in prompting hair growth after an injury and during the normal hair growth cycle.

“Skin repair after injury is a highly complex process,” said lead author Jessica L. Shannon, a graduate student in the departments of Dermatology and Immunology at Duke University School of Medicine. “TSLP does not show up immediately after injury, but appears about four days into the healing process. Previous studies described how TSLP triggers immune responses involved in tissue repair, so we initially questioned whether TSLP can speed up wound healing.”

Surprisingly, Shannon said, the molecule did not hasten wound repair. Instead, she and colleagues found that it interacted with stem cells residing in hair follicles, accelerating the onset of hair growth.

In laboratory studies using mice, the researchers found that an injection of TSLP between layers of the skin promoted hair growth. Conversely, when they neutralized the TSLP receptor in skin to block its action, hair growth after injury was inhibited.

“This work is a result of serendipitous observation that changed the direction of my thesis project and how we think about epithelial cell interactions with immune modulators during regeneration,” Shannon said.

Shannon said the research is now aiming to define the precise mechanisms involved, which could then lead to potential new approaches to harness the molecule to promote hair growth and regeneration.

In addition to Shannon, study authors include David L. Corcoran, John C. Murray, Steven F. Ziegler, Amanda S. MacLeod, and Jennifer Y. Zhang.

The study received support from the National Institute of Allergy and Infectious Diseases (R01-AI139207), the National Institute of Arthritis and Muscular Skeletal and Skin Diseases (R01-AR068991) and the Department of Dermatology of Duke University School of Medicine.

 

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