Hair, which is one of the distinguishing features of mammals, serves many essential biological functions, including thermoregulation, physical protection, sensory activity, and the distribution of sweat gland products, such as pheromones. Hair shafts are produced by thousands of hair follicles in mammalian skin, and these follicles continuously regenerate throughout life. The hair follicle represents a unique, highly regenerative system that physiologically undergoes cycles of growth (anagen), apoptosis-mediated regression (catagen), and rest (telogen) numerous times in life.

The EGFR/RAS/RAF/MEK/ERK pathway has a well-described role in skin and hair follicle development. Its function in the skin and its appendages, including hair follicles, is necessary for proper development and tissue homeostasis, and its deregulation rapidly results in defects in cellular proliferation and differentiation. The SHOC2 phosphatase complex, which comprises SHOC2, MRAS, and PP1, is a key regulatory node required for efficient RAS-RAF-MEK-ERK pathway activation. Here, we have used a conditional SHOC2 knockout mouse model to examine the effect of SHOC2 ablation on hair growth in adult mice. Our earlier findings demonstrate that when SHOC2 is systemically deactivated in adult mice, it leads to skin dermatitis and various histopathological changes, including an increased number of anagen-phase hair follicles within the hypodermis. Therefore, to investigate whether aberrant anagen-phase hair follicles affect hair growth, we depilated age-matched SHOC2 KO and WT male mice and monitored them for 28 days.

The results indicate that there were no significant differences in hair regeneration between SHOC2 KO and WT mice. This suggests that the increased number of hair follicles in the anagen phase in SHOC2 KO mice does not necessarily correlate with increased hair growth.