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MicroRNA-223 is involved in the pathogenesis of atopic dermatitis by affecting histamine-N-methyltransferase

Hui-Zhen Jia1, Sheng-Lin Liu1, Yan-Fen Zou2

  • 1Shenzhen Key Laboratory for Translational Medicine of Dermatology, Biomedical Research Institute, Shenzhen Peking University - the Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, Guangdong Province, China.

Cellular and Molecular Biology (Noisy-Le-Grand, France)
|March 7, 2018
PubMed

Insights

MicroRNAs (miRNAs) like miR-223 are upregulated in atopic dermatitis (AD). This study found miR-223 indirectly increases histamine-N-methyltransferase (HNMT) to degrade excess histamine in AD.

Area of Science:

  • Immunodermatology
  • Molecular Biology
  • Genetics

Background:

  • Atopic dermatitis (AD) is a widespread inflammatory skin condition.
  • Histamine is a key inflammatory mediator in AD pathogenesis.
  • MicroRNAs (miRNAs) are implicated in AD through gene regulation.

Purpose of the Study:

  • To investigate the role of miR-223 in atopic dermatitis.
  • To explore the relationship between miR-223 and histamine metabolism in AD.

Main Methods:

  • Quantification of miR-223 in whole blood cells from AD patients.
  • Measurement of histamine-N-methyltransferase (HNMT) in AD patients and mouse models.
  • Analysis of the miR-223 binding site on the HNMT gene.

Main Results:

  • miR-223 was found to be upregulated in the blood cells of AD patients.
  • HNMT, a histamine-degrading enzyme, was increased in AD patients and models.
  • Despite a potential binding site, miR-223 did not directly inhibit HNMT.

Conclusions:

  • miR-223 is upregulated in atopic dermatitis.
  • The study suggests miR-223 indirectly upregulates HNMT, leading to increased histamine degradation in AD.
Keywords:
Atopic dermatitisHistamine-N-methyltransferaseMicro RNAsmiR-223.

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