Evidence that geniposide abrogates norepinephrine-induced hypopigmentation by the activation of GLP-1R-dependent c-kit receptor signaling in melanocyte

Lan, Wen-Jun; Wang, Haiyan; Lan, Wei; Wang, Keyu; Rui-Ming, Wang

doi:10.1016/j.jep.2008.03.021

Cited by 18 publications

(11 citation statements)

References 29 publications

(26 reference statements)

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“…Melanin content was quantified using previously described methods (Friedmann and Gilchrest, 1987; Wen-Jun et al, 2008). Briefly, 2.5×10 5 melanocytes were collected and pelleted at 16,000xg for 30 seconds.…”

Section: Methodsmentioning

confidence: 99%

Modeling Neural Crest Induction, Melanocyte Specification, and Disease-Related Pigmentation Defects in hESCs and Patient-Specific iPSCs

et al. 2013

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SUMMARY Melanocytes are pigment-producing cells of neural crest origin responsible for protecting the skin against UV-irradiation. Pluripotent stem cell technology offers a novel approach for studying human melanocyte development and disease. Here we report that timed exposure to activators of WNT, BMP and EDN3 signaling triggers the sequential induction of neural crest and melanocyte precursor fates under dual-SMAD inhibition conditions. Using a SOX10::GFP hESC reporter line, we demonstrate that the temporal onset of WNT activation is particularly critical for human neural crest induction. Subsequent maturation of hESC-derived melanocytes yields pure populations matching the molecular and functional properties of adult melanocytes. Melanocytes from Hermansky-Pudlak and Chediak-Higashi Syndrome patient-specific iPSCs faithfully reproduce the ultrastructural features of disease-associated pigmentation defects. Our data define a highly specific requirement for WNT signaling during neural crest induction and enable the generation of pure populations of hiPSC-derived melanocytes for faithful modeling of human pigmentation disorders.

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Section: Methodsmentioning

confidence: 99%

Modeling Neural Crest Induction, Melanocyte Specification, and Disease-Related Pigmentation Defects in hESCs and Patient-Specific iPSCs

et al. 2013

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“…116,117 Genipin inhibited RANKL-induced osteoclast differentiation in bone marrow macrophages (BMMs) during culture by suppressing RANKL-induced IκB degradation along with mRNA expression of osteoclastic markers such as NFATc1, TRAP, and OSCAR and inhibition of c-Fos protein proteolysis in RANKL-treated BMMs. Genipin could be qualified to be a candidate for the treatment of osteoporosis.…”

Section: Miscellaneous Activitiesmentioning

confidence: 99%

Phytochemistry, Pharmacological Activities and Intellectual Property Landscape of Gardenia jasminoides Ellis: a Review

Phatak¹

2015

Phcog J

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“…The neural hypothesis suggested that accumulation of a neurochemical substance decreases melanin production. Abundant norepinephrine (NE) as an extrinsic factor secreted by nerve endings or keratinocytes leads to direct impairment of melanocytes differentiated from neural crest cells [16]. The link between vitiligo and the activity of monoaminergic systems has been found based on the finding that levels of norepinephrine (NE), epinephrine (E), normetanephrine (NMN), metanephrine (MN), homovanillic acid (HVA), and 5-hydroxyindolacetic acid (5-HIAA) were significantly higher in patients with vitiligo compared to controls [17].…”

Section: Introductionmentioning

confidence: 99%

Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes

Qiao

Wang

Xiang

et al. 2016

Oxidative Medicine and Cellular Longevity

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Vitiligo is a common chronic acquired pigmentation disorder characterized by loss of functional melanocytes from the epidermis and follicular reservoir. Among multiple hypotheses which have been proposed in the pathogenesis of vitiligo, autoimmunity and oxidative stress-mediated toxicity in melanocytes remain most widely accepted. Macroautophagy is a lysosome-dependent degradation pathway which widely exists in eukaryotic cells. Autophagy participates in the oxidative stress response in many cells, which plays a protective role in preventing damage caused by oxidative stress. Recent studies have enrolled autophagy as an important regulator in limiting damage caused by UV light and lipid oxidation, keeping oxidative stress in a steady state in epidermal keratinocytes and maintaining normal proliferation and aging of melanocytes. Impairment of autophagy might disrupt the antioxidant defense system which renders melanocytes to oxidative insults. These findings provide supportive evidence to explore new ideas of the pathogenesis of vitiligo and other pigmentation disorders.

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Evidence that geniposide abrogates norepinephrine-induced hypopigmentation by the activation of GLP-1R-dependent c-kit receptor signaling in melanocyte

Cited by 18 publications

References 29 publications

Modeling Neural Crest Induction, Melanocyte Specification, and Disease-Related Pigmentation Defects in hESCs and Patient-Specific iPSCs

Modeling Neural Crest Induction, Melanocyte Specification, and Disease-Related Pigmentation Defects in hESCs and Patient-Specific iPSCs

Phytochemistry, Pharmacological Activities and Intellectual Property Landscape of Gardenia jasminoides Ellis: a Review

Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes

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