title: Gene expression analysis of melanocortin system in vitiligo.
abstract: BACKGROUND
  The melanocortin system in the skin coordinates pigmentation and immune response and could be implicated in the pathogenesis of vitiligo.
  
  
  OBJECTIVE
  We aimed to analyze changes in expression of genes involved in skin pigmentation (melanocortin system and enzymes involved in melanin synthesis).
  
  
  METHODS
  With quantitative RT-PCR we measured the mRNA expression levels of eight genes from the melanocortin system and two enzymes involved in melanogenesis. RNA was extracted from both lesional and non-lesional skin of vitiligo patients and in non-sun-exposed skin of healthy subjects.
  
  
  RESULTS
  POMC (proopiomelanocortin) expression was lower in lesional skin compared to non-lesional skin. Expression of melanocortin receptors was increased in unaffected skin of vitiligo patients compared to healthy subjects and decreased in lesional skin compared to uninvolved skin of vitiligo patients, the differences were statistically significant in the cases of MC1R (melanocortin receptor 1) and MC4R (melanocortin receptor 4). TRP1 and DCT genes were down-regulated in lesional skin compared to non-lesional vitiligo skin or skin of healthy controls and up-regulated in uninvolved vitiligo skin compared to healthy control samples. In non-lesional skin, POMC expression was not elevated, possibly indicating that systemic influences are involved in up-regulation of MC receptor genes. Decreased expression of the analyzed genes in the lesional skin is not surprising, but statistically significant increased expression of studied genes in non-lesional skin from vitiligo patients is not described previously.
  
  
  CONCLUSIONS
  In our mind, up-regulation of melanocortin system in non-lesional skin could be systemic compensation to restore normal pigmentation in lesions.
authors.affiliation: Department of Dermatology and Venerology, Centre of Molecular and Clinical Medicine, University of Tartu, Estonia.
authors.forename: Külli
authors.initials: K
authors.lastname: Kingo
authors.forename: Eerik
authors.initials: E
authors.lastname: Aunin
authors.forename: Maire
authors.initials: M
authors.lastname: Karelson
authors.forename: Mari-Anne
authors.initials: MA
authors.lastname: Philips
authors.forename: Ranno
authors.initials: R
authors.lastname: Rätsep
authors.forename: Helgi
authors.initials: H
authors.lastname: Silm
authors.forename: Eero
authors.initials: E
authors.lastname: Vasar
authors.forename: Ursel
authors.initials: U
authors.lastname: Soomets
authors.forename: Sulev
authors.initials: S
authors.lastname: Kõks
mesh_terms: D000328:Adult; D000368:Aged; D054366:Agouti Signaling Protein / Q000235:genetics / Q000378:metabolism*; D054369:Agouti-Related Protein / Q000235:genetics / Q000378:metabolism*; D016022:Case-Control Studies; D005260:Female; D015870:Gene Expression; D006801:Humans; D008297:Male; D053486:Melanocortins / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D044101:Receptors, Melanocortin / Q000235:genetics / Q000378:metabolism*; D012867:Skin / Q000378:metabolism; D013312:Stress, Physiological / Q000378:metabolism; D014820:Vitiligo / Q000235:genetics / Q000378:metabolism*
chemical_list: D054366:Agouti Signaling Protein; D054369:Agouti-Related Protein; D053486:Melanocortins; D044101:Receptors, Melanocortin