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Published on: February 9, 2011
MicroRNA-939 amplifies Staphylococcus aureus-induced matrix metalloproteinase expression in atopic dermatitis
Jiating Wang1, Yejing Huang1, Xinfeng Wu1
1Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing, China.
Background:
Atopic dermatitis (AD) is a common chronic inflammatory skin diseases that seriously affects life quality of the patients. Staphylococcus aureus (S. aureus) colonization on the skin plays an important role in the pathogenesis of AD; however, the mechanism of how it modulates skin immunity to exacerbate AD remains unclear. MicroRNAs are short non-coding RNAs that act as post-transcriptional regulators of genes. They are involved in the pathogenesis of various inflammatory skin diseases.
Methods:
In this study, we established miRNA expression profiles for keratinocytes stimulated with heat-killed S. aureus (HKSA). The expression of miR-939 in atopic dermatitis patients was analyzed by fluorescence in situ hybridization (FISH). miR-939 mimic was transfected to human primary keratinocyte to investigate its impact on the expression of matrix metalloproteinase genes (MMPs) in vitro. Subsequently, miR-939, along with Polyplus transfection reagent, was administered to MC903-induced atopic dermatitis skin to assess its function in vivo.
Results:
MiR-939 was highly upregulated in HKSA-stimulated keratinocytes and AD lesions. In vitro studies revealed that miR-939 increased the expression of matrix metalloproteinase genes, including MMP1, MMP3, and MMP9, as well as the cell adhesion molecule ICAM1 in human primary keratinocytes. In vivo studies indicated that miR-939 increased the expression of matrix metalloproteinases to promote the colonization of S. aureus and exacerbated S. aureus-induced AD-like skin inflammation.
Conclusions:
Our work reveals miR-939 is an important regulator of skin inflammation in AD that could be used as a potential therapeutic target for AD.
Insights
MicroRNA-939 (miR-939) is upregulated in atopic dermatitis (AD) and promotes Staphylococcus aureus colonization by increasing matrix metalloproteinases. This finding highlights miR-939 as a potential therapeutic target for AD skin inflammation.
Area of Science:
- Dermatology
- Molecular Biology
- Immunology
Background:
- Atopic dermatitis (AD) is a chronic inflammatory skin condition impacting patient quality of life.
- Skin colonization by Staphylococcus aureus (S. aureus) is implicated in AD pathogenesis, but its immune modulation mechanisms are unclear.
- MicroRNAs (miRNAs) are key post-transcriptional regulators involved in inflammatory skin disease pathways.
Purpose of the Study:
- To investigate the role of microRNA expression in keratinocytes stimulated by S. aureus.
- To analyze the expression of miR-939 in atopic dermatitis patients.
- To determine the functional impact of miR-939 on skin immunity and S. aureus colonization in AD.
Main Methods:
- Generated miRNA expression profiles for keratinocytes exposed to heat-killed S. aureus (HKSA).
- Quantified miR-939 expression in AD lesions using fluorescence in situ hybridization (FISH).
- Utilized miR-939 mimic transfection in keratinocytes and in vivo models of AD to assess functional effects.
Main Results:
- miR-939 was significantly upregulated in HKSA-stimulated keratinocytes and AD skin lesions.
- In vitro, miR-939 increased the expression of matrix metalloproteinase genes (MMP1, MMP3, MMP9) and ICAM1 in keratinocytes.
- In vivo, miR-939 exacerbated S. aureus-induced AD-like skin inflammation by upregulating matrix metalloproteinases, promoting S. aureus colonization.
Conclusions:
- miR-939 acts as a critical regulator of skin inflammation in atopic dermatitis.
- The study identifies miR-939 as a potential therapeutic target for managing AD.
- Targeting miR-939 may offer a novel strategy for treating S. aureus-associated AD exacerbations.
