Keratinocyte-Targeted Overexpression of the Glucocorticoid Receptor Delays Cutaneous Wound Healing
Open accessAbstract
Delayed wound healing is one of the most common secondary adverse effects associated to the therapeutic use of glucocorticoid (GC) analogs, which act through the ligand-dependent transcription factor GC-receptor (GR). GR function is exerted through DNA-binding-dependent and -independent mechanisms, classically referred to as transactivation (TA) and transrepression (TR). Currently both TA and TR are thought to contribute to the therapeutical effects mediated by GR; however their relative contribution to unwanted side effects such as delayed wound healing is unknown. We evaluated skin wound healing in transgenic mice with keratinocyte-restricted expression of either wild type GR or a mutant GR that is TA-defective but efficient in TR (K5-GR and K5-GR-TR mice, respectively). Our data show that at days (d) 4 and 8 following wounding, healing in K5-GR mice was delayed relative to WT, with reduced recruitment of granulocytes and macrophages and diminished TNF-α and IL-1β expression. TGF-β1 and Kgf expression was repressed in K5-GR skin whereas TGF-β3 was up-regulated. The re-epithelialization rate was reduced in K5-GR relative to WT, as was formation of granulation tissue. In contrast, K5-GR-TR mice showed delays in healing at d4 but re-established the skin breach at d8 concomitant with decreased repression of pro-inflammatory cytokines and growth factors relative to K5-GR mice. Keratinocytes from both transgenic mice closed in vitro wounds slower relative to WT, consistent with the in vivo defects in cell migration. Overall, the delay in the early stages of wound healing in both transgenic models is similar to that elicited by systemic treatment with dexamethasone. Wound responses in the transgenic keratinocytes correlated with reduced ERK activity both in vivo and in vitro. We conclude that the TR function of GR is sufficient for negatively regulating early stages of wound closure, while TA by GR is required for delaying later stages of healing.
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Keratinocyte-targeted overexpression of GRs leads to delayed re-epithelialization and granulation tissue formation, with reduced pro-inflammatory cytokines and granulocyte/macrophage infiltration.
“keratinocyte-targeted overexpression of GRs leads to delayed re-epithelialization and granulation tissue formation, which is accompanied by reduced expression of pro-inflammatory cytokines and infiltration of granulocytes and macrophages in the wounds [139].”
From Transition from inflammation to proliferation: a critical step during wound healing (2016) · cites this paper as [139]
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- Authors
- Sanchis, A., Alba, L., Latorre, V., Sevilla, L. M., & Pérez, P.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Pérez, Paloma
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-01-03
- Volume
- 7
- Issue
- 1
- Pages
- e29701
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3250471
- OpenAlex
- W2066238445
- Cited by
- 35
- References
- 38
- Citations by year
- 2026: 3 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2018: 7 · 2017: 3 · 2016: 4 · 2015: 5 · 2014: 2 · 2013: 5
- FWCI
- 4.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- glucocorticoid receptor, delayed wound healing, keratinocytes, transrepression, transcriptional activation, glucocorticoid adverse effects, re-epithelialization, granulation tissue, TGF-β1, keratinocyte growth factor, TGF-beta3, TNF-α, IL-1β, ERK signaling, dexamethasone, cell migration
- MeSH terms
- Animals, Female, Gene Expression Regulation, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Receptors, Glucocorticoid, Skin, Wound Healing, Transcriptional Activation, Keratinocytes, Cytokines, Intercellular Signaling Peptides and Proteins, Mice
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