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Updated: Mar 20, 2026
Studying Chronic Exposure of Mice to Ultraviolet B Radiation
Published on: August 19, 2025
Identification of a novel PPARβ/δ/miR-21-3p axis in UV-induced skin inflammation
Gwendoline Degueurce1, Ilenia D'Errico1, Christine Pich1
1Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Abstract:
Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPARβ/δ is known to control mouse cutaneous repair and UV-induced skin cancer development. Here, we describe a novel PPARβ/δ-dependent molecular cascade involving TGFβ1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.
Insights
UV radiation triggers a novel molecular pathway in the skin involving PPARβ/δ and miR-21-3p, driving inflammation and potentially cancer. Inhibiting miR-21-3p offers a therapeutic avenue for UV-induced skin disorders.
Area of Science:
- Dermatology
- Molecular Biology
- Oncology
Background:
- Excessive UV exposure causes skin issues and cancer.
- Mechanisms of UV-induced inflammatory skin disorders are not fully understood.
- PPARβ/δ regulates skin repair and UV-induced cancer.
Purpose of the Study:
- To elucidate the molecular mechanisms of UV-induced inflammatory skin disorders.
- To identify novel molecular players in UV-induced skin responses.
- To explore therapeutic targets for UV-related skin conditions.
Main Methods:
- Investigated a PPARβ/δ-dependent molecular cascade in UV-exposed epidermis.
- Identified miR-21-3p as a novel UV-induced miRNA in keratinocytes.
- Assessed the role of miR-21-3p in UV-induced inflammation using ex vivo human skin.
Main Results:
- A novel PPARβ/δ-dependent cascade involving TGFβ1 and miR-21-3p is activated by UV exposure.
- miR-21-3p acts as a pro-inflammatory factor in keratinocytes and is elevated in psoriasis and squamous cell carcinomas.
- Inhibition of miR-21-3p decreased UV-induced cutaneous inflammation in human skin biopsies.
Conclusions:
- miR-21-3p is a key mediator of UV-induced skin inflammation and is implicated in skin diseases.
- Targeting miR-21-3p presents a potential therapeutic strategy for cutaneous disorders.
- miRNA-based topical therapies show clinical relevance for UV-induced skin conditions.
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