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miR-203 promotes HaCaT cell overproliferation through targeting LXR-α and PPAR-γ
Yueyuan Xiao1,2, Haizhen Wang1, Chang Wang1
1Department of Dermatology, the Second Affiliated Hospital, The Domestic First-class Discipline Construction Project of Chinese Medicine of Hunan University of Chinese Medicine , Changsha, Hunan 410005, China.
Abstract:
Psoriasis is an immune-mediated chronic inflammatory skin disease. Keratinocyte hyperproliferation has been regarded as a significant event in psoriasis pathogenesis. Considering the vital role of miRNA-mediated mRNA repression in psoriasis pathogenesis, in the present study, we attempted to investigate the mechanism of keratinocyte overproliferation from the point of miRNA-mRNA regulation. Both online microarray expression profiles and experimental results indicated that the expression of LXR-α and PPAR-γ was downregulated in psoriasis lesion skin. LXR-α or PPAR-γ overexpression alone was sufficient to inhibit keratinocyte proliferation, decrease KRT5 and KRT14 protein levels and increase KRT1 and KRT10 protein levels. miR-203 negatively regulated LXR-α and PPAR-γ expression through direct targeting. miR-203 inhibition exerted the opposite effects to LXR-α or PPAR-γ overexpression on HaCaT cells. More importantly, LXR-α or PPAR-γ overexpression could markedly remarkably attenuate the effects of miR-203 overexpression in keratinocytes, indicating that miR-203 promotes keratinocyte proliferation by targeting LXR-α and PPAR-γ. In conclusion, the miR-203-LXR-α/PPAR-γ axis modulates the proliferation of keratinocytes and might be a novel target for psoriasis treatment, which needs further in vivo investigation.
Insights
MicroRNA-203 (miR-203) promotes skin cell overgrowth in psoriasis by targeting LXR-alpha and PPAR-gamma. Inhibiting miR-203 may offer a new therapeutic strategy for psoriasis.
Area of Science:
- Dermatology
- Molecular Biology
- Gene Regulation
Background:
- Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation.
- MicroRNA (miRNA)-mediated gene regulation plays a critical role in psoriasis pathogenesis.
Purpose of the Study:
- To investigate the role of miRNA-mRNA interactions in keratinocyte overproliferation in psoriasis.
- To elucidate the mechanism by which miR-203 regulates keratinocyte proliferation via targeting LXR-alpha and PPAR-gamma.
Main Methods:
- Analysis of microarray expression profiles and experimental validation.
- Overexpression and inhibition studies of miR-203, LXR-alpha, and PPAR-gamma in keratinocytes.
- Assessment of keratinocyte proliferation and protein levels of KRT5, KRT14, KRT1, and KRT10.
Main Results:
- LXR-alpha and PPAR-gamma expression were downregulated in psoriatic skin lesions.
- miR-203 directly targets and downregulates LXR-alpha and PPAR-gamma.
- miR-203 overexpression promoted keratinocyte proliferation, while its inhibition reduced proliferation.
- LXR-alpha or PPAR-gamma overexpression counteracted the proliferative effects of miR-203.
Conclusions:
- The miR-203-LXR-alpha/PPAR-gamma axis is a key regulator of keratinocyte proliferation in psoriasis.
- This axis represents a potential novel therapeutic target for psoriasis treatment.
- Further in vivo studies are warranted to validate these findings.
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