The dermal stem cell factor and c-kit are overexpressed in melasma

• Published in: British journal of dermatology (1951) Vol. 154; no. 6; pp. 1094 - 1099
• Main Authors: Kang, H.Y., Hwang, J.S., Lee, J.Y., Ahn, J.H., Kim, J-Y., Lee, E-S., Kang, W.H.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.06.2006; Blackwell; Oxford University Press
• Subjects: Adult; Biological and medical sciences; c-kit; Dermatology; dermis; Fibroblasts - pathology; Humans; Medical sciences; Melanosis - metabolism; Melanosis - pathology; melasma; Pigmentary diseases of the skin; Proto-Oncogene Proteins c-kit - biosynthesis; Proto-Oncogene Proteins c-kit - genetics; Proto-Oncogene Proteins c-kit - metabolism; Reverse Transcriptase Polymerase Chain Reaction - methods; RNA, Messenger - genetics; Skin - metabolism; Skin - pathology; stem cell factor; Stem Cell Factor - biosynthesis; Stem Cell Factor - genetics; Stem Cell Factor - metabolism; Up-Regulation; Human; Skin disease; Chloasma; Pigmentation disorder; stem cell factor; Dermatology; c-kit; dermis; C-Onc gene; melasma; Derm; Mast cell growth factor; kit Gene
• ISSN: 0007-0963; 1365-2133
• DOI: 10.1111/j.1365-2133.2006.07179.x

Summary Background  The pathogenesis of melasma has not yet been clearly demonstrated. We tried to determine whether the stem cell factor (SCF) and its receptor c‐kit are involved in the mechanism of hyperpigmentation of melasma because this factor is highly implicated in the stimulation of melanocyte function in vitro and in vivo. Objectives  The present study was conducted to investigate the expression of SCF and c‐kit on the lesions of melasma compared with nonlesional skin. Patients/methods  Skin samples were obtained from lesional and nonlesional facial skin of 60 Korean women with melasma. Immunohistochemistry and reverse transcriptase‐polymerase chain reaction (RT‐PCR) analysis was performed to determine the expression of SCF and c‐kit in melasma. Results  The expression of SCF was significantly increased at the lesional dermis compared with nonlesional dermis. However, there was no significant difference in the expression of SCF in lesional and nonlesional epidermis. The expression of c‐kit was significantly increased at lesional epidermis compared with nonlesional skin. RT‐PCR of SCF and c‐kit mRNAs demonstrated increased expression of both types of transcripts in the lesional skin compared with nonlesional skin. Conclusions  These results suggest that the increased expression of SCF in the dermis and of c‐kit in the epidermis play an important role in the mechanism of hyperpigmentation in melasma.