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July 28, 2020
What goosebumps are for
At a Glance
- Researchers discovered a new role for goosebumps: the muscle and nerve cells involved in this response to cold trigger new hair growth by activating stem cells.
- These mechanisms may have implications for reversing hair loss and understanding wound healing in the skin.
Even though humans have evolved to have relatively little body hair, we still produce goosebumps when cold. Goosebumps occur when tiny muscles in our skin’s hair follicles, called arrector pili muscles, pull hair upright.
For animals with thick fur, this response helps keep them warm. But it doesn’t do so for people. Still, this ability to make goosebumps persists in humans and other animals that don’t have enough hair to retain warmth.
Researchers led by Drs. Ya-Chieh Hsu from Harvard University and Sung-Jan Lin from National Taiwan University used skin samples from mice to explore what other roles goosebumps might play. Previous research identified a trio of cell types that work together to create goosebumps: arrector pili muscles, sympathetic nerves, and the hair follicles.
The work was funded in part by NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results were published on July 15, 2020, in Cell.
The team first used drugs and genetic models to remove sympathetic nerves from the skin. In response, hair follicle stem cells were slow to activate and new hair production was delayed.
Further experiments showed that removing sympathetic nerves reduced the amount of a chemical called norepinephrine in the skin. Norepinephrine is a type of neurotransmitter—a substance that nerve cells use to communicate. When the team produced mice with hair follicle stem cells that lacked the receptor for norepinephrine, activation of the stem cells was delayed, similar to when sympathetic nerves were removed.
The researchers next used electron microscopy to generate extremely high-resolution pictures of the hair follicles. The sympathetic nerves were not only intertwined with muscle, but also interacted with the stem cells. Further imaging showed that the ends of the nerves and the stem cells formed synapses, which let cells communicate chemically.
Finally, the team teased out the role of the muscle cells in the follicles. They used two different techniques to destroy arrector pili muscle in the skin while leaving nerves and stem cells intact. Without the muscle cells, connections between the nerves and stem cells were lost, and the mice showed a delay in both stem cell activation and production of new hair.
Based on these results, the researchers proposed that the muscle cells form a bridge between the nerve and the stem cells in the hair follicle. In this way, goosebumps might play two roles: They cause hair to rise in the short term and trigger more hair growth by the stem cells in the long term.
To test this idea, the researchers compared mice exposed to either cold or normal room temperatures. The cold exposure first caused goosebumps, then boosted activity in the sympathetic nerves and an increase in norepinephrine. Mice exposed to the cold started to produce new hairs from their stem cells in less than two weeks.
“It’s a two-layer response: goosebumps are a quick way to provide some sort of relief in the short term. But when the cold lasts, this becomes a nice mechanism for the stem cells to know it’s maybe time to regenerate new hair coat,” says Dr. Yulia Shwartz, a postdoctoral researcher in the Hsu lab who is first author of the study.
Arrector pili muscle cells are often lost in the scalps of people with common baldness. Finding a way to reactivate the sympathetic nerves in hair follicles despite this loss may provide a way to boost hair growth. The team is also interested in studying whether these interactions might play a role in other processes in the skin, such as wound healing.
—by Sharon Reynolds
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References: Cell Types Promoting Goosebumps Form a Niche to Regulate Hair Follicle Stem Cells. Shwartz Y, Gonzalez-Celeiro M, Chen CL, Pasolli HA, Sheu SH, Fan SM, Shamsi F, Assaad S, Lin ET, Zhang B, Tsai PC, He M, Tseng YH, Lin SJ, Hsu YC. Cell. 2020 Jul 15:S0092-8674(20)30808-4. doi: 10.1016/j.cell.2020.06.031. Online ahead of print. PMID: 32679029.
Funding: NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); New York Stem Cell Foundation; Smith Family Foundation Odyssey Award; Pew Charitable Trusts; Harvard NeuroDiscovery Center; Harvard Stem Cell Institute; Harvard Medical School Dean’s Innovation Grant; American Cancer Society; Taiwan Ministry of Science and Technology; National Taiwan University Hospital; Taiwan Bio-Development Foundation; Helen Hay Whitney Foundation; Weizmann Institute of Science; Simmons University; American Diabetes Association; Charles A. King Trust; National Science Foundation.