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Updated: Dec 12, 2025

Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
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Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model

Published on: September 7, 2013

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Targeting steroid receptor RNA activator (SRA), a long non-coding RNA, enhances melanogenesis through activation of

Ji-Chen Ho1,2, Chih-Hung Lee1, Chien-Hui Hong3,4

  • 1Department of Dermatology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Plos One
|August 14, 2020
PubMed

Insights

Steroid receptor RNA activator (SRA) influences skin pigmentation by regulating the p38-TRP1 pathway. Targeting SRA may offer new treatments for pigmentary diseases.

Area of Science:

  • Molecular Biology
  • Dermatology
  • Genetics

Background:

  • Melanin homeostasis is crucial for skin health, and its disruption causes pigmentary diseases.
  • Melanogenesis is a complex process influenced by genetic, environmental, and epigenetic factors.
  • Steroid receptor RNA activator (SRA), a long noncoding RNA, is implicated in steroidogenesis and cancer but its role in melanogenesis is unexplored.

Purpose of the Study:

  • To investigate the role of SRA in regulating melanogenesis and skin pigmentation.
  • To elucidate the molecular mechanisms underlying SRA's function in melanin production.
  • To assess the therapeutic potential of targeting SRA for pigmentary disorders.

Main Methods:

  • RNA interference (RNAi) was used to knockdown SRA expression in B16 and A375 melanoma cell lines.
  • Gene and protein expression levels of melanogenesis-related factors (TRP1, TRP2) were analyzed.
  • Western blotting was employed to assess p38 phosphorylation.
  • Pharmacological inhibition of p38 was performed using SB202190.

Main Results:

  • SRA knockdown in B16 cells led to increased pigmentation and elevated TRP1 and TRP2 expression.
  • SRA knockdown inhibited constitutive p38 phosphorylation in B16 cells.
  • Inhibition of p38 in B16 cells mimicked the effect of SRA knockdown, increasing melanin content.
  • In A375 cells, SRA RNAi resulted in reduced p38 phosphorylation, increased TRP1 expression, and hypermelanosis.

Conclusions:

  • The SRA-p38-TRP1 axis plays a significant role in regulating melanin homeostasis.
  • SRA acts as a regulator of melanogenesis through the p38 signaling pathway.
  • SRA represents a potential therapeutic target for managing refractory pigmentary diseases.

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