Search

Background: There is a growing interest in the relationship among stress hormones, neuroendocrine signaling, and skin diseases, including hair loss. Previous reports showed that stress hormones inhibit human hair growth and induce early catagen transition. Moreover, a CRH receptor antagonist reversed CRH‐induced alopecia in a mouse model, suggesting that antagonization of the CRH receptor is a key clinical strategy to treat stress‐induced hair loss. Objectives: The aim of this study was to investigate the protective effect of CRH receptor antagonists from Pulsatilla chinensis on human hair follicles (hHFs) and human dermal papilla cells (hDPCs). Methods: hHFs were observed and scored by hair cycle. The levels of cAMP, a second messenger, were measured in each group. In addition, the mRNA and protein levels of factors related to the hair cycle were measured. Furthermore, the expression levels of various members of the mitogen‐activated protein kinase (MAPK) signaling pathway related to stress were measured. Results: CRH induced early catagen transition in an ex vivo hair organ culture model. In addition, CRH downregulated the levels of alkaline phosphatase (ALP) and hair anagen‐related cytokines in cultured hDPCs. Moreover, CRH induced the phosphorylation of JNK, c‐Jun, p38, ERK, and Akt in cultured hDPCs. CRH receptor antagonists isolated from P chinensis reversed these CRH‐induced modulations in both ex vivo hair follicles (HFs) and cultured hDPCs. Conclusions: These results indicate that P chinensis effectively blocks CRH receptor function and that saponin derivatives from P chinensis could be a pharmaceutical and cosmetic approach to treat stress‐induced hair loss. [ABSTRACT FROM AUTHOR]

Background: Stress is an important cause of skin disease, including hair loss. The hormonal response to stress is due to the HPA axis, which comprises hormones such as corticotropin releasing factor (CRF), adrenocorticotropic hormone (ACTH), and cortisol. Many reports have shown that CRF, a crucial stress hormone, inhibits hair growth and induces hair loss. However, the underlying mechanisms are still unclear. The aim of this study was to examine the effect of CRF on human dermal papilla cells (DPCs) as well as hair follicles and to investigate whether the HPA axis was established in cultured human DPCs. Results: CRF inhibited hair shaft elongation and induced early catagen transition in human hair follicles. Hair follicle cells, both human DPCs and human ORSCs, expressed CRF and its receptors and responded to CRF. CRF inhibited the proliferation of human DPCs through cell cycle arrest at G2/M phase and induced the accumulation of reactive oxygen species (ROS). Anagen-related cytokine levels were downregulated in CRF-treated human DPCs. Interestingly, increases in proopiomelanocortin (POMC), ACTH, and cortisol were induced by CRF in human DPCs, and antagonists for the CRF receptor blocked the effects of this hormone. Conclusion: The results of this study showed that stress can cause hair loss by acting through stress hormones. Additionally, these results suggested that a fully functional HPA axis exists in human DPCs and that CRF directly affects human DPCs as well as human hair follicles under stress conditions. [ABSTRACT FROM AUTHOR]