The DOI matches its Crossref record; 33 of the 34 references it cites were found in a registry or an index.
Dexamethasone Induction of Keloid Regression through Effective Suppression of VEGF Expression and Keloid Fibroblast Proliferation
Open accessAbstract
The biological mechanism underlying steroid therapy for treating keloids remains unclear. Analytical results demonstrated that topical intra-lesional steroid injections suppress vascular endothelial growth factor (VEGF) expression in keloid tissue and induce its regression in vivo. This study investigated whether glucocorticoid (dexamethasone) downregulates VEGF expression and hinders keloid fibroblast (KF) proliferation in keloid regression. Primary KF cultures were treated with various concentrations of dexamethasone, glucocorticoid receptor (GR) antagonist (mifeprostone, RU-486), VEGF-A antibody, VEGF receptor-2 (VEGF-R2) antagonist (SU-5416), and VEGF protein. Analytical results demonstrated that dexamethasone retarded KFs proliferation. However, suppression of fibroblast proliferation by dexamethasone pre-treatment was reduced by adding exogenous VEGF protein. Dexamethasone suppressed endogenous VEGF mRNA induction, protein expressed by KFs, and angiogenesis activity detected by a tube-forming assay of human umbilical vein endothelial cells co-cultured fibroblasts. These effects were reversed by pre-treatment with RU-486, and not by pre-treatment with SU-5416. Thus, dexamethasone induces keloid regression via interaction with the GR and suppresses endogenous VEGF expression and fibroblast proliferation. However, exogenous VEGF promotes fibroblast proliferation through the GR-independent pathway. Modulation of VEGF production may comprise a valuable treatment modality for keloids.
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“glucocorticoids including DX have been shown to decrease the in vivo activity of VEGF.207–209”
From Biocompatible Materials for Continuous Glucose Monitoring Devices (2013) · cites this paper as [209]
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Metadata
- Authors
- Wu, W.-S., Wang, F.-S., Yang, K. D., Huang, C.-C., & Kuo, Y.-R.
- Affiliations
- Chang Gung University (TW)
- Corresponding author
- Kuo, Yur-Ren
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2006-06
- Volume
- 126
- Issue
- 6
- Pages
- 1264-1271
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2147641426
- Cited by
- 174
- References
- 34
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 10 · 2023: 6 · 2022: 14 · 2021: 12 · 2020: 9 · 2019: 6 · 2018: 8 · 2017: 8 · 2016: 12 · 2015: 10 · 2014: 7 · 2013: 10 · 2012: 6
- FWCI
- 4.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Pittsburgh
- National Science Council
- Topics
- Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Health Sciences › Medicine › Surgery › Vascular Malformations and Hemangiomas
- Keywords
- dexamethasone, glucocorticoid therapy, vascular endothelial growth factor, VEGF-A, keloid fibroblasts, fibroblast proliferation, glucocorticoid receptor, RU486, angiogenesis
- MeSH terms
- Antibodies, Monoclonal, Cells, Cultured, Dexamethasone, Fibroblasts, Glucocorticoids, Humans, Keloid, Receptors, Glucocorticoid, RNA, Messenger, Umbilical Cord, Mifepristone, Vascular Endothelial Growth Factor Receptor-2, Vascular Endothelial Growth Factor A, Endothelial Cells, Cell Proliferation
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