Hair growth‐promotion effects of different alternating current parameter settings are mediated by the activation of Wnt/<i>β</i>‐catenin and <scp>MAPK</scp> pathway

Sohn, Ki Min; Jeong, Kwan; Kim, Jung Eun; Park, Young Min; Kang, Hoon

doi:10.1111/exd.12827

Cited by 35 publications

(26 citation statements)

References 18 publications

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“…AKT, a downstream effector of phosphatidylinositol 3-kinase, is implicated in growth and survival of a variety of cells ( Hers et al, 2011 ). Activation of AKT appears to contribute to hair growth ( Sohn et al, 2015 ; Woo et al, 2017 ). Numerous studies have reported that EGCG regulates AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…The sonic hedgehog (Shh) and protein kinase B (AKT) signaling pathways are essential for the development and growth of hair follicles and transition between anagen and telogen ( St-Jacques et al, 1998 ; Wang et al, 2000 ; Sohn et al, 2015 ). Activation of the Shh or AKT signals can enhance the proliferation of hair follicle cells and promote hair growth ( Li et al, 2015 ; Lin et al, 2015 ; Sohn et al, 2015 ; Woo et al, 2017 ). EGCG has been demonstrated to trigger Shh signaling pathway in hippocampus of adult mice and enhance the hippocampal neurogenesis ( Wang et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

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Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways

et al. 2018

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Background: Hair follicles play an essential role in the growth of hair. Epigallocatechin-3-gallate (EGCG), a catechin polyphenol in green tea, has various bioactivities. The present study aims to evaluate the effect of EGCG on the growth of mink hair follicles and investigate the possible molecular mechanisms.Methods: The length of hair follicles was recorded up to 6 days in presence of 0.1–5 μM EGCG. Primary dermal papilla cells (DPCs) and outer root sheath cells (ORSCs) were treated with 0.25–4 μM EGCG, and their growth was evaluated by MTT assay and cell cycle detection. The levels of key molecules in sonic hedgehog (Shh) and protein kinase B (AKT) signaling pathways were further assessed by quantitative real-time PCR, western blot and immunofluorescence. To determine the involvement of Shh and AKT pathways in EGCG-mediated growth-promotion of ORSCs and DPCs, Shh pathway inhibitors cyclopamine and GANT61 or AKT pathway inhibitor LY294002 were employed, and then cell proliferation and cell cycle were analyzed.Results: Data from ex vivo culture showed that, in presence of 0.5–2.5 μM EGCG, the growth of mink hair follicles was promoted. In vitro, the proliferation of DPCs and ORSCs was enhanced by 0.5–4 μM EGCG treatment. More cells entered S phase upon treatment of EGCG, accompanied with upregulation of cyclin D1 and cyclin E1. Furthermore, when exposed to EGCG, the Shh and AKT signaling pathways were activated in both hair follicles and primary DPCs and ORSCs. Inhibiting either of these two pathways partly reversed the effect of EGCG on proliferation and cell cycle of DPCs and ORSCs.Conclusion: EGCG promotes the growth of mink hair follicles at concentrations of 0.5–2.5 μM. This growth-promoting effect of EGCG may be associated with the increased proliferation of DPCs and ORSCs through activating Shh and AKT signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways

et al. 2018

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“…In addition, electromagnetic field resulted in stimulation of DPCs activity . Electrical stimulation also induced hair regrowth by inducing hair follicular proliferation and stimulation of DPCs in vitro .…”

Section: Hair Growth Promoting Effectmentioning

confidence: 99%

Review of Hair Follicle Dermal Papilla cells asin vitroscreening model for hair growth

Madaan

Verma

Singh

et al. 2018

Intern J of Cosmetic Sci

113

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Hair disorders such as hair loss (alopecia) and androgen dependent, excessive hair growth (hirsutism, hypertrichosis) may impact the social and psychological well-being of an individual. Recent advances in understanding the biology of hair have accelerated the research and development of novel therapeutic and cosmetic hair growth agents. Preclinical models aid in dermocosmetic efficacy testing and claim substantiation of hair growth modulators. The in vitro models to investigate hair growth utilize the hair follicle Dermal Papilla cells (DPCs), specialized mesenchymal cells located at the base of hair follicle that play essential roles in hair follicular morphogenesis and postnatal hair growth cycles. In this review, we have compiled and discussed the extensively reported literature citing DPCs as in vitro model to study hair growth promoting and inhibitory effects. A variety of agents such as herbal and natural extracts, growth factors and cytokines, platelet-rich plasma, placental extract, stem cells and conditioned medium, peptides, hormones, lipid-nanocarrier, light, electrical and electromagnetic field stimulation, androgens and their analogs, stress-serum and chemotherapeutic agents etc. have been examined for their hair growth modulating effects in DPCs. Effects on DPCs' activity were determined from untreated (basal) or stress induced levels. Cell proliferation, apoptosis and secretion of growth factors were included as primary end-point markers. Effects on a wide range of biomolecules and mechanistic pathways that play key role in the biology of hair growth were also investigated. This consolidated and comprehensive review summarizes the up-to-date information and understanding regarding DPCs based screening models for hair growth and may be helpful for researchers to select the appropriate assay system and biomarkers. This review highlights the pivotal role of DPCs in the forefront of hair research as screening platforms by providing insights into mechanistic action at cellular level, which may further direct the development of novel hair growth modulators.

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“…MAP kinase-signaling pathway has been shown to be involved in the proliferation and migration of skin keratinocytes and fibroblasts [ 42 , 43 , 44 ]. To investigate the effects of visfatin on the activation of MAP kinases in HDFs, cells were treated with visfatin and phosphorylation of each MAP kinase was determined by western blot analysis.…”

Section: Resultsmentioning

confidence: 99%

Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway

Lee

Song

Lee

et al. 2018

IJMS

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Visfatin, a member of the adipokine family, plays an important role in many metabolic and stress responses. The mechanisms underlying the direct therapeutic effects of visfatin on wound healing have not been reported yet. In this study, we examined the effects of visfatin on wound healing in vitro and in vivo. Visfatin enhanced the proliferation and migration of human dermal fibroblasts (HDFs) and keratinocytes the expression of wound healing-related vascular endothelial growth factor (VEGF) in vitro and in vivo. Treatment of HDFs with visfatin induced activation of both extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinases 1 and 2 (JNK1/2) in a time-dependent manner. Inhibition of ERK1/2 and JNK1/2 led to a significant decrease in visfatin-induced proliferation and migration of HDFs. Importantly, blocking VEGF with its neutralizing antibodies suppressed the visfatin-induced proliferation and migration of HDFs and human keratinocytes, indicating that visfatin induces the proliferation and migration of HDFs and human keratinocytes via increased VEGF expression. Moreover, visfatin effectively improved wound repair in vivo, which was comparable to the wound healing activity of epidermal growth factor (EGF). Taken together, we demonstrate that visfatin promotes the proliferation and migration of HDFs and human keratinocytes by inducing VEGF expression and can be used as a potential novel therapeutic agent for wound healing.

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Hair growth‐promotion effects of different alternating current parameter settings are mediated by the activation of Wnt/β‐catenin and MAPK pathway

Cited by 35 publications

References 18 publications

Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways

Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways

Review of Hair Follicle Dermal Papilla cells asin vitroscreening model for hair growth

Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway

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