Baldness is reversible
Researchers from Harvard University have found that the stress hormone transfers the stem cells of hair follicles into a phase of prolonged rest, stopping the regeneration of hair. In experiments on mice, they identified a specific cell type and protein responsible for transmitting stress signals to stem cells, and showed that targeting this pathway can be used to restore hair growth.
The hair follicle is one of the few mammalian tissues that can undergo regeneration cycles throughout life. Thanks to the stem cells of the hair follicles, the processes of growth and rest naturally alternate. During the growth phase, stem cells are activated to regenerate the follicle, and the hair grows and thickens. In the resting phase, the stem cells are in a state of sleep, and the hair is thinning and falling out. Hair loss is caused by the fact that stem cells remain dormant without entering the active phase of regeneration.
Mouse hair follicle. The cells of the dermal papilla (green) produce the Gas6 molecule, which activates the stem cells of the hair follicle.
The researchers created a mouse model of chronic stress and found that the stem cells of hair follicles remain in the resting phase for a very long time without tissue regeneration. The main stress hormone in mice is corticosterone (an analog of human cortisol), it is produced by the adrenal glands; by injecting corticosterone into mice, the researchers reproduced the stress effect on stem cells.
Under normal conditions, the regeneration of hair follicles slows down with age – the resting phase becomes longer as the animals age. But when the researchers removed the stress hormone, the resting phase of the stem cells became extremely short, and the stem cells constantly entered the growth phase to regenerate hair follicles, even when the mice were old.
Having established a link between the stress hormone and the activity of hair follicle stem cells, the researchers began to search for the biological mechanism underlying this connection.
To determine whether the stress hormone regulates stem cells directly, the researchers removed the corticosterone receptor, but instead of the expected increase in hair growth, the accumulation of dermal cells in the dermal papilla under the hair follicle began.
It is known that the dermal papilla is important for the activation of hair follicle stem cells, but none of the known factors secreted by the cells of the dermal papilla has changed with a decrease in the influence of stress hormone levels. Corticosterone inhibited the expression of a specific growth arrest gene Gas6 in the cells of the dermal papilla, which activates the stem cells of hair follicles that were previously in the resting phase.
Under both normal and stressful conditions, the expression of Gas6 led to the activation of hair follicle stem cells. These initial results in mice need further confirmation before they can be safely applied to humans.
Recently , scientists from Columbia University has found out how stress affects another type of stem cells in the hair follicle – melanocyte stem cells that regenerate hair pigment. Researchers have shown that stress activates the sympathetic nervous system and depletes melanocyte stem cells, which leads to premature graying of hair. The new study proved that although stress has a negative effect on both hair follicle stem cells and melanocyte stem cells, the mechanisms of this effect are different. Stress depletes melanocyte stem cells directly through nerve signals, while the activation of hair follicles is prevented indirectly through the action of the adrenal stress hormone on the cells of the dermal papilla. Since the stem cells of the hair follicles are not depleted, it may be possible to reactivate them under stress using the Gas6 mechanism.
Article S.Choi et al. Corticosterone inhibits GAS6 to govern hair follicle stem-cell quiescence published in the journal Nature.
Aminat Adzhieva, portal "Eternal Youth" http://vechnayamolodost.ru based on The Harvard Gazette: How chronic stress leads to hair loss.