ArticleExperimental dermatology2021
Keratinocyte-derived IL-1β induces PPARG downregulation and PPARD upregulation in human reconstructed epidermis following barrier impairment.
Article in Experimental dermatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Comprehensive analysis of phenotypes and transcriptome characteristics reveal important contribution of chronic stress and inflammation in the pathogenesis of acne.Bioscience reports · 2026Article
- Epidermal PPARγ Signaling as a Suppressor of Toll-like Receptor-Mediated Inflammation and Fibrosis: Relevance to Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- PPARα deficiency causes skin dysbiosis and triggers innate immunity in keratinocytes.Cell death & disease · 2026Article
- PPARγ: a key orchestrator of epidermal barrier, immune responses, and lipid metabolism in atopic dermatitis pathogenesis and therapy.Frontiers in allergy · 2026Review
- IL-1β-induced STAT3 activation drives IL-17-producing CD8Journal of translational medicine · 2025Article
- The antibacterial activity and therapeutic potential of the amphibian-derived peptide TB_KKG6K.mSphere · 2025Article
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- MAPK14 as a key gene for regulating inflammatory response and macrophage M1 polarization induced by ferroptotic keratinocyte in psoriasis.Inflammation · 2024Article
- New Insights into the Role of PPARγ in Skin Physiopathology.Biomolecules · 2024Review
- The role of PPAR in fungal keratitis.Frontiers in immunology · 2024Review
- Emphasis on Adipocyte Transformation: Anti-Inflammatory Agents to Prevent the Development of Cancer-Associated Adipocytes.Cancers · 2023Review
- Up-Regulated Expression of ICAM1, MT1A, PTGS2, LCE3D, PPARD, and GM-CSF2 Following Solar Skincare Protection and Repair Strategies in a 3-Dimensional Reconstructed Human Skin Model.Clinical, cosmetic and investigational dermatology · 2023Article
- Identification of Novel Hub Genes Associated with Psoriasis Using Integrated Bioinformatics Analysis.International journal of molecular sciences · 2022Article
- Small, Cationic Antifungal Proteins from Filamentous Fungi InhibitMicrobiology spectrum · 2022Article
- Mechanism of Huoluo Xiaoling Dan in the Treatment of Psoriasis Based on Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Peroxisomal Fatty Acid Oxidation and Glycolysis Are Triggered in Mouse Models of Lesional Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2021Article
- PPARdelta in Affected Atopic Dermatitis and Psoriasis: A Possible Role in Metabolic Reprograming.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Peroxisome proliferator-activated receptors (PPARs) are a family of nuclear hormone receptors. In skin, PPARs modulate inflammation, lipid synthesis, keratinocyte differentiation and proliferation and thus are important for skin barrier homeostasis. Accordingly, PPAR expression is altered in various skin conditions that entail epidermal barrier impairment, that is atopic dermatitis (AD) and psoriasis. Using human epidermal equivalents (HEEs), we established models of acute epidermal barrier impairment devoid of immune cells. We assessed PPAR and cytokine expression after barrier perturbation and examined effects of keratinocyte-derived cytokines on PPAR expression. We show that acetone or SDS treatment causes graded impairment of epidermal barrier function. Furthermore, we demonstrate that besides IL-1β and TNFα, IL-33 and TSLP are highly relevant markers for acute epidermal barrier impairment. Both SDS- and acetone-mediated epidermal barrier impairment reduce PPARG expression levels, whereas only SDS enhances PPARD expression. In line with findings in IL-1β and TNFα-treated HEEs, abrogation of IL-1 signalling restores PPARG expression and limits the increase of PPARD expression in SDS-induced epidermal barrier impairment. Thus, following epidermal barrier perturbation, keratinocyte-derived IL-1β and partly TNFα modulate PPARG and PPARD expression. These results emphasize a role for PPARγ and PPARβ/δ in acute epidermal barrier impairment with possible implications for diseases such as AD and psoriasis.
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