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MicroRNA-125a Correlates with Decreased Psoriasis Severity and Inflammation and Represses Keratinocyte Proliferation
Fang Su1,2, Liang Jin3, Wei Liu4
1Department of Dermatology, The First Hospital of China Medical University, Shenyang, China.
Background:
Psoriasis has a complex etiology related to inflammation and dysregulated immune system. MicroRNA (miR)-125a is a miRNA intimately related to inflammation and immunity; therefore, we presumed that it might play a role in the pathogenesis of psoriasis. This study aimed to investigate the correlation of miR-125a with disease severity and inflammation in psoriasis patients, and the effect of miR-125a on proliferation, apoptosis as well as its target signaling pathway in keratinocytes.
Methods:
Sixty psoriasis patients were consecutively recruited, then lesional and non-lesional skin tissue samples were collected. miR-125a in lesional and non-lesional skin tissues, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-17 mRNA expressions in lesional skin tissues were detected. Then, miR-125a overexpression, control overexpression, miR-125a knockdown and control knockdown plasmids were transfected into HaCaT cells. Subsequently, cell proliferation, apoptosis, IL-23R, JAK2, and STAT3 expressions were assessed.
Results:
miR-125a was reduced in lesional skin tissue compared with non-lesional skin tissue (p < 0.001), and it distinguished lesional skin tissue from non-lesional skin tissue with a high area under curve of 0.917 (95% CI 0.866-0.968). Negative association of miR-125a in lesional skin tissue with lesional body surface area (p = 0.037) and psoriasis area and severity index score (p < 0.001) was found. Additionally, miR-125a was negatively correlated with TNF-α (p = 0.001), IL-1β (p = 0.014), and IL-17 (p = 0.003) in lesional skin tissue. In cellular experiments, miR-125a overexpression inhibited proliferation and promoted apoptosis, while miR-125a knockdown enhanced proliferation and repressed apoptosis in HaCaT cells. Additionally, miR-125a negatively regulated the IL-23R/JAK2/STAT3 pathway in HaCaT cells.
Conclusion:
miR-125a could facilitate the disease monitoring and probably has the potential to be a therapeutic target in psoriasis.
Insights
MicroRNA-125a is reduced in psoriatic skin and correlates with disease severity. Lower miR-125a levels promote keratinocyte proliferation and inhibit apoptosis, suggesting its therapeutic potential for psoriasis.
Area of Science:
- Dermatology
- Molecular Biology
- Immunology
Background:
- Psoriasis involves complex inflammation and immune dysregulation.
- MicroRNA-125a (miR-125a) is linked to inflammation and immunity.
- The role of miR-125a in psoriasis pathogenesis was investigated.
Purpose of the Study:
- To examine the correlation between miR-125a and psoriasis severity.
- To assess miR-125a's impact on keratinocyte proliferation and apoptosis.
- To explore miR-125a's effect on target signaling pathways.
Main Methods:
- Collected skin samples from 60 psoriasis patients.
- Quantified miR-125a, TNF-α, IL-1β, IL-6, and IL-17 mRNA.
- Utilized HaCaT cells for in vitro experiments with miR-125a manipulation.
Main Results:
- miR-125a was significantly reduced in lesional psoriatic skin.
- Reduced miR-125a correlated with increased disease severity and inflammation markers (TNF-α, IL-1β, IL-17).
- miR-125a modulated keratinocyte proliferation, apoptosis, and the IL-23R/JAK2/STAT3 pathway.
Conclusions:
- miR-125a levels are associated with psoriasis.
- miR-125a may serve as a biomarker for disease monitoring.
- miR-125a presents a potential therapeutic target for psoriasis treatment.
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