Melanogenesis During the Anagen-Catagen-Telogen Transformation of the Murine Hair Cycle

Słomiński, Andrzej; Paus, Ralf; Płonka, Przemysław M.; Chakraborty, Ashok; Maurer, Marcus; Pruski, Daniel; Lukiewicz, Stanislaw

doi:10.1111/1523-1747.ep12382606

Cited by 164 publications

(173 citation statements)

References 39 publications

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“…Melanocytes begin to shut down melanogenesis in late anagen and regression phase called catagen, and it die by apoptosis on the hair bulb in rest phase called telogen. The melanogenesis in melanocytes reappears when hair follicles reenter anagen [7][8][9][10]. The prevention of melanogenesis in the hair bulb on anagen is induced by the aging or stress which results in gray hair.…”

Section: Melanin Biosynthesismentioning

confidence: 99%

Effect of quercetin derivatives on melanogenesis stimulation of melanoma cells

Mitsunaga

Yamauchi

2015

J Wood Sci

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Controlling melanogenesis is important for maintaining the good health and cosmetic appearance of a human body. This study aims to search the active compounds from natural products exhibiting the melanogenesis modulating activity and elucidate the mechanism underlying the observed activity. Two novel quercetin glycosideswere isolated and identified from Helminthostachys zeylanica roots 50 % ethanol extract. Compound 1 exhibited intracellular melanogenesis stimulatory activity, while 2 showed no effect even the structural similarity. To understand the structure-activity relationships, twelve quercetin glycosides and seven methylquercetins were synthesized from rutin as starting material. As the result of bioassay using synthesized nineteen quercetin derivatives in B16 melanoma cells, some quercetin-3-O-b-D-glucopyranosides stimulated the intracellular melanogenesis. On the other hand, synthesized 3-O-methylquercetin 12 and 3,4 0 ,7-Otrimethylquercetin 15 increased both intra and extracellular melanin contents with no cytotoxicity. Compoud 15 increased the phosphorylated p38 mitogen-activated protein kinase (MAPK) and microphthalmia-associated transcription factor (MITF) which regulates the expression of tyrosinase, TRP-1 and TRP-2. While 12 enhanced the expression of the melanogenic enzymes without involving the MITF, as evidenced by its lack of any stimulation of the expression of MITF and p-p38 MAPK. This result indicates that 12 may stimulate the expression of tyrosinase, TRP-1, and TRP-2 by stimulating currently unidentified transcriptional factors and/or by regulating the degradation of melanogenic enzymes.

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Section: Melanin Biosynthesismentioning

confidence: 99%

Effect of quercetin derivatives on melanogenesis stimulation of melanoma cells

Mitsunaga

Yamauchi

2015

J Wood Sci

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“…Peeling off the wax/rosin mixture removes all hair shafts and immediately induces a highly synchronized hair growth. 38,40,41 …”

Section: Anagen Inductionmentioning

confidence: 99%

Neurogenic Inflammation in Stress-Induced Termination of Murine Hair Growth Is Promoted by Nerve Growth Factor

Peters

Handjiski

Kuhlmei

et al. 2004

The American Journal of Pathology

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Recently, we have revealed the existence of a "brainhair follicle axis" in murine skin and have identified the neuropeptide substance P (SP) as a key mediator of stress-induced hair growth inhibition in vivo. Published evidence suggests that increased numbers of SP-immunoreactive sensory fibers, as seen in the dermis of stressed mice in anagen-catagen transition, are a result of transient high levels of nerve growth factor (NGF). Thus, we now aimed at dissecting the role of NGF in stress-triggered hair growth termination in our murine model. By real time PCR and immunohistochemistry, stress-exposed mice showed an up-regulation of NGF and its low-affinity receptor p75NTR; the NGF high-affinity receptor TrkA was moderately down-regulated. On neutralization of NGF, premature onset of catagen, apoptosis, and increased number/ activation of perifollicular mast cells and antigen-presenting cells, which reflects the skin response to stress, was significantly abrogated. Stress or subcutaneous injection of recombinant NGF (to mimic stress) resulted in an increased percentage of SP ؉ neurons in dorsal root ganglia, as measured by retrograde tracing. Taken together, these data suggest that NGF is a central element in the perifollicular neurogenic inflammation that develops during the murine skin response to stress and antagonizing NGF may be a promising therapeutic approach to counter the negative effect of stress on hair growth. Recently, we have introduced a mouse model launching experimental evidence that stress-induced hair loss is fact, and not fiction, as every so often imputed by a number of dermatologists. This mouse model provides new insights into the pathophysiology of stress-induced hair growth inhibition and permits exploration of various strategies for therapeutic intervention. 1,2 In this model, exposure to sonic stress inhibits the growth of a hair shaft producing (anagen) hair follicle by premature induction of hair follicle regression (catagen) and up-regulated keratinocyte apoptosis. At the same time, it induces neurogenic inflammation characterized by perifollicular mast cell degranulation and accumulation of antigen-presenting cells, eg, activated macrophages. 3 The neuropeptide substance P (SP) was identified as a key mediator of stress-induced hair growth inhibition, since increased number of SP-immunreactive nerve fibers were present in the skin of stressed mice and hair growth inhibition could be blocked by SP-receptor antagonists.

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“…It has also been reported that hair pigmentation, which requires c-Kit as a receptor protein tyrosine kinase (Nishikawa et al, 1991), may be coupled to the anagen phase of the hair cycle (Slominski and Paus, 1993;Slominski et al, 1994;Ortonne and Prora, 1993), although not all anagen phases accompany pigmentation. In black-haired skin, the termination of melanogenesis is one of the earliest signs of catagen induction, and melanogenesis is absent throughout telogen (Slominski and Paus, 1993;Slominski et al, 1994;Ortonne and Prora, 1993). This raises a possibility that the melanin production-promoting RET somehow regulates hair growth cycle.…”

Section: Introductionmentioning

confidence: 98%

RET tyrosine kinase enhances hair growth in association with promotion of melanogenesis

et al. 2001

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We ®rst demonstrated that c-Ret protein is transiently expressed mainly in the inner and outer root sheaths of hair follicles soon after birth in the skin of normal C57BL/6 and BALB/c mice. A longer-lasting expression of activated RET protein overlapped the c-Ret expression with some preferential expression in the outer root sheath in close association with increase in the number of S-100 protein-containing cells in the area and excess melanogenesis in and around hair bulbs in the skin of RFP-RET-transgenic mice on a C57BL/6 background (RFP-RET/B6). Hair follicles in the skin of the transgenic mice continuously showed histology of the anagen phase, and the recovery period for the hair of the transgenic mice after shaving was shortened. Such growth promotion was not observed in the case of white hairs of RFP-RET-transgenic mice on a BALB/c background. These results suggest that RET works to extend the anagen phase in association with upregulation of melanin production. Oncogene (2001) 20, 7536 ± 7541.

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Melanogenesis During the Anagen-Catagen-Telogen Transformation of the Murine Hair Cycle

Cited by 164 publications

References 39 publications

Effect of quercetin derivatives on melanogenesis stimulation of melanoma cells

Effect of quercetin derivatives on melanogenesis stimulation of melanoma cells

Neurogenic Inflammation in Stress-Induced Termination of Murine Hair Growth Is Promoted by Nerve Growth Factor

RET tyrosine kinase enhances hair growth in association with promotion of melanogenesis

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