Detection of melanocyte lineage-specific genes in vitiligo lesions.

Abstract:

:Vitiligo is an acquired pigmentary disorder characterized by the loss of skin color and functional melanocytes. The pathogenesis of vitiligo remains unclear, which means that effective clinical treatment is difficult. However, if melanocyte linkage-specific genes are identified in vitiligo lesions, the appropriate treament for melanocytes may be implemented. The current study aimed to detect the expression of melanocyte lineage-specific genes in vitiligo lesion needle biopsies and to predict the occurrence of perifollicular repigmentation in depigmented macules. A total of 6 patients with stable vitiligo and 4 healthy volunteers were recruited from the Department of Dermatology, Wuhan Third Hospital. Total RNA was extracted from skin tissue needle biopsies from the periphery and center of depigmented macules, and adjacent normal skin. The expression of dopachrome tautomerase (Dct), tyrosinase (Tyr) and β-actin (ACTB) genes were detected using a reverse transcription (RT)-semi quantitative polymerase chain reaction (PCR) assay. RNA extracted from 7 mg of skin samples was sufficient to amplify all three genes. The expression profile of each patient was then observed in the center of vitiligous lesions and were deemed to be Dct+Tyr-ACTB+, Dct-Tyr-ACTB+ or Dct+Tyr+ACTB+. At 5 months, patient follow-up indicated that perifollicular repigmentation was efficaciously induced by 308 nm eximer light radiation in a patient who had a Dct+Tyr-ACTB+ gene expression. The results demonstrated that needle skin biopsy and RT-semi quantitative PCR may be used as a less traumatic and reliable method to detect the expression profiles of melanocyte lineage-specific genes in needle biopsies, which may have the potential to predict the occurrence of perifollicular repigmentation in vitiligo.

journal_name

Exp Ther Med

authors

Xu W,Wang X

doi

10.3892/etm.2019.7496

subject

Has Abstract

pub_date

2019-06-01 00:00:00

pages

4485-4491

issue

6

eissn

1792-0981

issn

1792-1015

pii

ETM-0-0-7496

journal_volume

17

pub_type

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