The Protease-Activated Receptor 2 Regulates Pigmentation via Keratinocyte-Melanocyte Interactions

Seiberg, Miri; Paine, Christine; Sharlow, Elizabeth R.; Andrade‐Gordon, Patricia; Costanzo, Michael J.; Eisinger, Magdalena; Shapiro, Stanley S.

doi:10.1006/excr.1999.4692

Cited by 216 publications

(217 citation statements)

References 30 publications

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“…Only twoand three-dimensional keratinocyte-melanocyte co-cultures treated with the PAR-2-activating peptide SLIGRL or with STI showed increased or decreased pigment deposition, respectively. The finding that PAR-2 is expressed by keratinocytes, but not by melanocytes (26), could explain the requirement for a keratinocyte -melanocyte contact for the PAR-2-induced pigmentary effects.…”

Section: Par-2 Affects Pigmentationmentioning

confidence: 95%

“…Epidermal equivalents containing melanocytes respond to PAR-2 activation by darkening, similar to their response following UVB irradiation (26). Trypsin inhibitors, known to inhibit PAR-2 cleavage [e.g., soybean trypsin inhibitor (STI) (38)], completely inhibited the UVB-induced pigmentation of these equivalents (26).…”

Section: Par-2 Affects Pigmentationmentioning

confidence: 99%

“…Trypsin inhibitors, known to inhibit PAR-2 cleavage [e.g., soybean trypsin inhibitor (STI) (38)], completely inhibited the UVB-induced pigmentation of these equivalents (26). Keratinocyte-melanocyte contact was required for the PAR-2-mediated pigmentary effects.…”

Section: Par-2 Affects Pigmentationmentioning

confidence: 99%

“…Keratinocytes treated with increasing doses of UVB irradiation were found to secrete protease activity, which cleaved a peptide comprising the PAR-2 cleavage site in a dose-dependent manner (41). Since the inhibition of PAR-2 activation prevents UVB-induced pigmentation in vitro (26), the contribution of the PAR-2 pathway to UV-mediated responses was examined in vivo. UV-induced tanning of Yucatan swine was prevented with topical treatments of STI-containing compositions ( Fig.…”

Section: Uvb Irradiation Induces Par-2 Activationmentioning

confidence: 99%

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Keratinocyte–Melanocyte Interactions During Melanosome Transfer

Seiberg¹

2001

Pigment Cell Research

243

185

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The epidermal-melanin unit is composed of one melanocyte sis theory. PAR-2 controls melanosome ingestion and phagocytosis by keratinocytes and exerts a regulatory role in skin and approximately 36 neighboring keratinocytes, working in pigmentation. Modulation of PAR-2 activity can enhance or synchrony to produce and distribute melanin. Melanin is decrease melanosome transfer and affects pigmentation only synthesized in melanosomes, transferred to the dendrite tips, when there is keratinocyte -melanocyte contact. Moreover, and translocated into keratinocytes, forming caps over the keratinocyte nuclei. The molecular and cellular mechanisms PAR-2 is induced by UV irradiation and inhibition of PAR-2 activation results in the prevention of UVB-induced tanning. involved in melanosome transfer and the keratinocytemelanocyte interactions required for this process are not yetThe role of PAR-2 in mediating UV-induced responses remains to be elucidated. completely understood. Suggested mechanisms of melanosome transfer include melanosome release and endocytosis, direct inoculation ('injection'), keratinocyte-melanocyte membrane Key words: Melanosome transfer, PAR-2, Phagocytosis, Keratinocyte, Melanocyte fusion, and phagocytosis. Studies of the keratinocyte receptor protease-activated receptor-2 (PAR-2) support the phagocytonisms for melanosome transfer. These include the release of melanosomes into intercellular spaces followed by endocytosis, direct inoculation ('injection'), keratinocyte -melanocyte membrane fusion, and phagocytosis. Using time-lapse microscopy, Okazaki et al. (7) observed dendrites enfolded by recipient keratinocytes, which are then pinched off to form a cluster of melanosomes. The internalized dendrites were decomposed, leaving each melanosome aggregate surrounded by a single keratinocyte membrane. Single large melanosomes, or complexes of small melanosomes, were then dispersed from the aggregate into the keratinocyte cytoplasm, in a skin-type-dependent process defined as cytophagocytosis. Electron microscopy studies of photo-damaged Caucasian facial skin (8) suggested a similar mechanism, as well as keratinocyte -melanocyte membrane fusion, and exocytosis of single melanosomes (reviewed in (5)). However, a mechanistic understanding of the cellular interactions involved in pigment transfer has not been described.

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Section: Par-2 Affects Pigmentationmentioning

confidence: 95%

Section: Par-2 Affects Pigmentationmentioning

confidence: 99%

Section: Par-2 Affects Pigmentationmentioning

confidence: 99%

Section: Uvb Irradiation Induces Par-2 Activationmentioning

confidence: 99%

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Keratinocyte–Melanocyte Interactions During Melanosome Transfer

Seiberg¹

2001

Pigment Cell Research

243

185

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“…Such defibrillation works only about two-thirds of the time and often damages the heart in the process of reviving it [10]. In external defibrillation, electrical shocks (≃ 5 kV) are applied across the patient's chest; they depolarise all heart cells simultaneously and essentially reset the pacemaking nodes of the heart [11]. Slightly lower voltages (≃ 600 V) suffice in open-heart conditions, i.e., when the shock is applied directly on the heart's surface [12].…”

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confidence: 99%

Defibrillation via the Elimination of Spiral Turbulence in a Model for Ventricular Fibrillation

2001

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Ventricular fibrillation (VF), the major reason behind sudden cardiac death, is turbulent cardiac electrical activity in which rapid, irregular disturbances in the spatiotemporal electrical activation of the heart makes it incapable of any concerted pumping action. Methods of controlling VF include electrical defibrillation as well as injected medication. Both methods yield results that are subject to chance. Electrical defibrillation, though widely used, involves subjecting the whole heart to massive, and often counterproductive, electrical shocks. We propose a defibrillation method that uses a very-low-amplitude shock (of order mV) applied for a brief duration (of order 100 ms) and over a coarse mesh of lines on our model ventricle. Our proposal is based on a detailed numerical study of a model for ventricular fibrillation [1].

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Melanosome Trafficking and Transfer

Scott¹

2006

The Pigmentary System

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The Protease-Activated Receptor 2 Regulates Pigmentation via Keratinocyte-Melanocyte Interactions

Cited by 216 publications

References 30 publications

Keratinocyte–Melanocyte Interactions During Melanosome Transfer

Keratinocyte–Melanocyte Interactions During Melanosome Transfer

Defibrillation via the Elimination of Spiral Turbulence in a Model for Ventricular Fibrillation

Melanosome Trafficking and Transfer

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