Hair loss is a common disorder associated with hair thinning and loss of hair from the head, caused by a variety of factors, including stress, inflammation, hormonal imbalance, nutritional imbalance, diseases, and medication ( Springer et al., 2003). Hair plays an important role in biological functions, from providing protection to maintaining body temperature (Kim and Dao, 2020). Our results suggest that MA promotes anagen signaling via autophagy and cell cycle progression by activating the Wnt/β-catenin and ERK pathways in DPCs. MA-induced ERK phosphorylation led to changes in the expression levels of Cdc2, Atg7 and LC3II, as well as DPC proliferation. On the other hand, MA increased the levels of phospho (Thr 202/Tyr 204)-extracellular signal regulated kinases (ERK). Moreover, XAV939 reduced MA-induced effects on cell cycle progression, autophagy, and DPC proliferation. Treatment with XAV939, an inhibitor of the Wnt/β-catenin pathway, attenuated the MA-induced increase in β-catenin nuclear translocation. MA also increased the phosphorylation levels of Wnt/β-catenin proteins, such as GSK3β (Ser 9) and β-catenin (Ser 552 and Ser 675). MA induced autophagosome formation by decreasing the levels of the phospho-mammalian target of rapamycin (phospho-mTOR) and increasing autophagy-related 7 (Atg7) and microtubule-associated protein 1A/1B-light chain 3II (LC3II). To elucidate the mechanism by which MA promotes DPC proliferation, we evaluated the effect of MA on autophagy and intracellular pathways. MA significantly increased DPC proliferation and stimulated the G2/M phase, accompanied by increasing cyclin A, Cdc2, and cyclin B1. In this study, we evaluated the effects of MA on anagen-activating signaling pathways in DPCs. However, the action mechanisms of MA on the stimulation of anagen signaling in DPCs is not known. Myristoleic acid (MA) increases Wnt reporter activity in DPCs. Dermal papilla cells (DPCs) regulate the hair cycle and play important roles in hair growth and regeneration. Alopecia is a distressing condition caused by the dysregulation of anagen, catagen, and telogen in the hair cycle.
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