ArticleThe British journal of dermatology2009
Interleukin (IL)-6 modulates transforming growth factor-beta expression in skin and dermal fibroblasts from IL-6-deficient mice.
Article in The British journal of dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 78 citations in OpenAlex.
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- Topical Administration of Heat-KilledBiomedicines · 2021Article
- Interleukin-6 promotes migration and extracellular matrix synthesis in retinal pigment epithelial cells.Histochemistry and cell biology · 2020Article
- Comprehensive Review of Hybrid Collagen and Silk Fibroin for Cutaneous Wound Healing.Materials (Basel, Switzerland) · 2020Review
- Hydroxyapatite Particles Induced Modulation of Collagen Expression and Secretion in Primary Human Dermal Fibroblasts.International journal of nanomedicine · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInterleukin (IL-6) and transforming growth factor (TGF)-beta have been shown to play a role in skin development and maintenance.
objectivesA link between these two cytokines has yet to be identified and therefore in this study we investigated the modulation of TGF-beta1 and TGF-beta type 2 receptor (TGF-betaR2) by IL-6 in skin.
methodsAn IL-6 knockout (IL-6KO) fibroblast-populated lattice model and intradermal injections of IL-6 into unwounded IL-6KO mice were used to investigate the direct effects of IL-6 treatment on TGF-beta and TGF-betaR2 expression and to determine the signalling mechanism. In addition, IL-6KO and C57BL/6 control mice were wounded by a 4-mm punch biopsy to monitor expression of TGF-beta1 and TGF-betaR2 within a wound over time. The expression of TGF-beta1 and TGF-betaR2 was assessed by real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assay and immunohistology.
resultsRecombinant IL-6 treatment of IL-6KO lattices and intradermal injections of IL-6 showed a significant induction of TGF-beta1 mRNA and protein, with TGF-beta1 expression localized in the dermis, while TGF-betaR2 expression was primarily in the epidermis in IL-6KO mice. During healing, the expression of TGF-beta1 and TGF-betaR2 mRNA was significantly greater in unwounded and 7-day-old wounds from wild-type mice; however, protein expression did not differ. Treatment with signal transduction inhibitors indicated that IL-6 modulates TGF-beta through a mitogen-activated protein kinase/extracellular signal-regulated kinase (Mapk/Erk)-dependent mechanism.
conclusionThese studies indicate that IL-6 has the ability to modulate the expression of TGF-beta and TGF-betaR2 to varying degrees in the skin, which may provide a possible mechanism for defining the role of IL-6 in skin maintenance and a new association of IL-6 with TGF-beta in pathologies associated with fibrosis.
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