ArticleThe Journal of biological chemistry2011
Cortisol synthesis in epidermis is induced by IL-1 and tissue injury.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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Who cites it
92 citing papers in PubMed, 190 citations in OpenAlex.
- Trial
- The role of the mineralocorticoid receptor in skin.Molecular and cellular endocrinology · 2025Review
- Enkephalin-producing regulatory T cells in the skin restrain local inflammation through control of nociception.Science immunology · 2025Article
- Neuro-immuno-endocrinology of the skin: how environment regulates body homeostasis.Nature reviews. Endocrinology · 2025Review
- Parainflammation in the Ocular System: Considerations on the Underlying Mechanisms and Treatment of Dry Eye Disease.Ophthalmology and therapy · 2025Review
- The Impact of Psychological Stress on Wound Healing: Implications for Neocollagenesis and Scar Treatment Efficacy.Clinical, cosmetic and investigational dermatology · 2025Review
- Dermal glucocorticoids are uncoupled from stress physiology and infection.Conservation physiology · 2025Article
- Review of sensory systems deployed by epidermal keratinocytes.Frontiers in cell and developmental biology · 2025Review
- Untargeted Metabolomic Analysis Reveals Plasma Differences between Mares with Endometritis and Healthy Ones.Animals : an open access journal from MDPI · 2024Article
- Host-Microbiome Crosstalk in Chronic Wound Healing.International journal of molecular sciences · 2024Review
- Therapeutic Effects of Statins: Promising Drug for Topical and Transdermal Administration.Current medicinal chemistry · 2024Review
- Tumors produce glucocorticoids by metabolite recycling, not synthesis, and activate Tregs to promote growth.The Journal of clinical investigation · 2023Article
- Effects and Stress-Relieving Mechanisms of Dark Tea Polysaccharide in Human HaCaT Keratinocytes and SZ95 Sebocytes.Molecules (Basel, Switzerland) · 2023Article
- Loss of epidermal glucocorticoid receptor protects against whole body metabolic dysfunction upon chronic corticosterone treatment.Molecular metabolism · 2023Article
- Acute stress response on Atlantic salmon: a time-course study of the effects on plasma metabolites, mucus cortisol levels, and head kidney transcriptome profile.Fish physiology and biochemistry · 2023Article
- The NIDDK Diabetic Foot Consortium.Journal of diabetes science and technology · 2023Article
- Skin 11β-hydroxysteroid dehydrogenase type 1 enzyme expression regulates burn wound healing and can be targeted to modify scar characteristics.Burns & trauma · 2023Article
- Neuroendocrine signaling in the skin with a special focus on the epidermal neuropeptides.American journal of physiology. Cell physiology · 2022Review
- Optimization of process parameters for fabrication of electrospun nanofibers containing neomycin sulfate andDrug delivery · 2022Article
- Controlling skin microbiome as a new bacteriotherapy for inflammatory skin diseases.Inflammation and regeneration · 2022Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Glucocorticoids (GCs) are known inhibitors of wound healing. In this study we report the novel finding that both keratinocytes in vitro and epidermis in vivo synthesize cortisol and how this synthesis regulates wound healing. We show that epidermis expresses enzymes essential for cortisol synthesis, including steroid 11 β-hydroxylase (CYP11B1), and an enzyme that controls negative feedback mechanism, 11β-hydroxysteroid dehydrogenase 2 (11βHSD2). We also found that cortisol synthesis in keratinocytes and skin can be stimulated by ACTH and inhibited by metyrapone (CYP11B1 enzyme inhibitor). Interestingly, IL-1β, the first epidermal signal of tissue injury, induces the expression of CYP11B1 and increases cortisol production by keratinocytes. Additionally, we found induction of CYP11B1 increased production of cortisol and activation of GR pathway during wound healing ex vivo and in vivo using human and porcine wound models, respectively. Conversely, inhibition of cortisol synthesis during wound healing increases IL-1β production, suggesting that cortisol synthesis in epidermis may serve as a local negative feedback to proinflammatory cytokines. Local GCs synthesis, therefore, may provide control of the initial proinflammatory response, preventing excessive inflammation upon tissue injury. Inhibition of GC synthesis accelerated wound closure in vivo, providing the evidence that modulation of cortisol synthesis in epidermis may be an important regulatory mechanism during wound healing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.