A team at the University of California, Irvine, has identified a signaling molecule that
potently stimulates hair growth.
SCUBE3 has been found to be a potential therapeutic option for treating androgenetic alopecia.
A signaling molecule known as SCUBE3, which was discovered by researchers at the University of California, Irvine, has the potential to cure androgenetic alopecia, a prevalent type of hair loss in both women and men.
The research, which was recently published in the journal Developmental Cell, uncovered the precise mechanism by which the dermal papilla cells, specialized signal-producing fibroblasts found at the bottom of each hair follicle, encourage new development. Although the critical role dermal papilla cells play in regulating hair growth is widely established, the genetic basis of the activating chemicals involved is little understood.
“At different times during the hair follicle life cycle, the very same dermal papilla cells can send signals that either keep follicles dormant or trigger new hair growth,” said Maksim Plikus, Ph.D., UCI professor of developmental & cell biology and the study’s corresponding author.
“We revealed that the SCUBE3 signaling molecule, which dermal papilla cells produce naturally, is the messenger used to ‘tell’ the neighboring hair stem cells to start dividing, which heralds the onset of new hair growth.”
For mice and humans to effectively develop hair, the dermal papilla cells must produce activating chemicals. Dermal papilla cells malfunction in people with androgenetic alopecia, drastically lowering the typically plentiful activating chemicals.
For mice and humans to effectively develop hair, the dermal papilla cells must produce activating chemicals. Dermal papilla cells malfunction in people with androgenetic alopecia, drastically lowering the typically plentiful activating chemicals.
For this study, a mouse model with excessive hair and hyperactivated dermal papilla cells was created. This model will help researchers learn more about the regulation of hair growth. READ MORE...