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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