Source:http://linkedlifedata.com/resource/pubmed/id/18426410
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
2008-4-22
|
| pubmed:abstractText |
The protease-activated receptor-2 (PAR-2) is a seven transmembrane G-protein-coupled receptor that could be activated by serine protease cleavage or by synthetic peptide agonists. We showed earlier that activation of PAR-2 with Ser-Leu-Ile-Gly-Arg-Leu-NH(2) (SLIGRL), a known PAR-2 activating peptide, induces keratinocyte phagocytosis and increases skin pigmentation, indicating that PAR-2 regulates pigmentation by controlling phagocytosis of melanosomes. Here, we show that Leu-Ile-Gly-Arg-NH(2) (LIGR) can also induce skin pigmentation. Both SLIGRL and LIGR increased melanin deposition in vitro and in vivo, and visibly darkened human skins grafted onto severe combined immuno-deficient (SCID) mice. Both SLIGRL and LIGR stimulated Rho-GTP activation resulting in keratinocyte phagocytosis. Interestingly, LIGR activates only a subset of the PAR-2 signaling pathways, and unlike SLIGRL, it does not induce inflammatory processes. LIGR did not affect many PAR-2 signaling pathways, including [Ca(2+)] mobilization, cAMP induction, the induction of cyclooxgenase-2 (COX-2) expression and the secretion of prostaglandin E2, interleukin-6 and -8. PAR-2 siRNA inhibited LIGR-induced phagocytosis, indicating that LIGR signals via PAR-2. Our data suggest that LIGR is a more specific regulator of PAR-2-induced pigmentation relative to SLIGRL. Therefore, enhancing skin pigmentation by topical applications of LIGR may result in a desired tanned-like skin color, without enhancing inflammatory processes, and without the need of UV exposure.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
1755-1471
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
21
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
172-83
|
| pubmed:dateRevised |
2009-12-11
|
| pubmed:meshHeading |
pubmed-meshheading:18426410-Administration, Topical,
pubmed-meshheading:18426410-Animals,
pubmed-meshheading:18426410-Blotting, Western,
pubmed-meshheading:18426410-Cells, Cultured,
pubmed-meshheading:18426410-Female,
pubmed-meshheading:18426410-Gene Silencing,
pubmed-meshheading:18426410-Humans,
pubmed-meshheading:18426410-Inflammation,
pubmed-meshheading:18426410-Keratinocytes,
pubmed-meshheading:18426410-Mice,
pubmed-meshheading:18426410-Mice, SCID,
pubmed-meshheading:18426410-Peptides,
pubmed-meshheading:18426410-Phagocytosis,
pubmed-meshheading:18426410-Receptor, PAR-2,
pubmed-meshheading:18426410-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18426410-Signal Transduction,
pubmed-meshheading:18426410-Skin Pigmentation,
pubmed-meshheading:18426410-Skin Transplantation,
pubmed-meshheading:18426410-Swine,
pubmed-meshheading:18426410-Transplantation, Heterologous
|
| pubmed:year |
2008
|
| pubmed:articleTitle |
LIGR, a protease-activated receptor-2-derived peptide, enhances skin pigmentation without inducing inflammatory processes.
|
| pubmed:affiliation |
The Johnson & Johnson Skin Research Center, Consumer Product Worldwide, A division of Johnson & Johnson Consumer Companies, Inc., 199 Grandview Rd., Skillman, NJ 08558, USA.
|
| pubmed:publicationType |
Journal Article
|