title: Intraepidermal nerve fibers increase in dry skin of acetone-treated mice.
abstract: BACKGROUND
  Skin dryness is apparent in several pruritic skin diseases, such as xerosis and atopic dermatitis. Our previous study has demonstrated an increase of nerve fibers in the epidermis of patients with xerosis, suggesting the contribution of nerve fibers to itching.
  
  
  OBJECTIVE
  This study was conducted to reveal a direct linkage between dry skin and intraepidermal nerve growth.
  
  
  METHODS
  ICR mice treated with acetone were used as a dry skin model. Time-dependent measurement of transepidermal water loss (TEWL) and stratum corneum (SC) hydration was performed on the treated areas. Moreover, both the distribution of intraepidermal nerve fibers and the expression of epidermal nerve growth factor (NGF) and amphiregulin (AR) were examined sequentially with immunohistochemistry and quantitative RT-PCR. The same experiments were carried out in control mice treated with sterile water.
  
  
  RESULTS
  Enhanced TEWL and decreased SC hydration were observed in the acetone-treated skins during the first hour after the treatment. These parameters gradually returned to the normal range within 48 h. In the acetone-treated mice, we found that there were many nerve fibers in the epidermis between 16 and 48 h after the treatment. No changes of the parameters for barrier disruption and intraepidermal nerve growth were observed in the control skins. Moreover, the expression of epidermal NGF and AR at the protein and mRNA levels was increased before the penetration of nerve fibers into the epidermis.
  
  
  CONCLUSIONS
  These results suggest that increases of epidermal NGF and AR levels are associated with intraepidermal nerve growth in acetone-treated mice.
authors.affiliation: Institute for Environmental and Gender Specific Medicine, Juntendo University Graduate School of Medicine, Department of Dermatology, and Urayasu Hospital, Tomioka, Urayasu, Chiba 279-0021, Japan.
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Tominaga
authors.forename: Sumiko
authors.initials: S
authors.lastname: Ozawa
authors.forename: Suhandy
authors.initials: S
authors.lastname: Tengara
authors.forename: Hideoki
authors.initials: H
authors.lastname: Ogawa
authors.forename: Kenji
authors.initials: K
authors.lastname: Takamori
mesh_terms: D000096:Acetone; D066258:Amphiregulin; D000818:Animals; D066255:EGF Family of Proteins; D004817:Epidermis / Q000294:innervation* / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism*; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009412:Nerve Fibers / Q000502:physiology*; D020932:Nerve Growth Factor / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014870:Water Loss, Insensible / Q000502:physiology*
chemical_list: D066258:Amphiregulin; C587849:Areg protein, mouse; D066255:EGF Family of Proteins; D006023:Glycoproteins; D036341:Intercellular Signaling Peptides and Proteins; D012333:RNA, Messenger; D000096:Acetone; D020932:Nerve Growth Factor