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Published on: August 3, 2018
Transforming growth factor-β1 in plaque morphea
Aleksandra Dańczak-Pazdrowska1, Michał J Kowalczyk1, Beata Szramka-Pawlak1
1Department of Dermatology, Poznan University of Medical Sciences, Poznan, Poland. Head of Department: Prof. Zygmunt Adamski MD, PhD.
Introduction:
Morphea (localized scleroderma) is a rare cutaneous disease characterized by skin fibrosis of unknown pathogenesis. Transforming growth factor-β (TGF-β) is a potent profibrotic factor. The role of TGF-β in morphea remains unclear.
Aim:
The goal of this study was to estimate the expression level of TGF-β1 in skin and peripheral blood mononuclear cells as well as the plasma levels of TGF-β1 in plaque morphea (MEP).
Material And Methods:
The study involved 20 MEP patients. Three control groups were involved: 1 - plasma: 36 healthy volunteers; 2 - PBMC: 47 healthy volunteers; 3 - skin biopsies: 13 samples collected during mastectomy (breast cancer was not skin involved). The analysis of TGF-β1 plasma levels was performed with the use an adequate ELISA kit, while real-time polymerase chain reaction was employed for the expression of TGF-β1 in peripheral blood mononuclear cells (PBMC) and skin.
Results:
In our study we have not detected differences in TGF-β 1 expression in PBMC, skin, nor in plasma levels of TGF-β1 between MEP patients and healthy controls, regardless of disease activity and its duration.
Conclusions:
The results of our study contradict the claim of the substantial role of TGF-β1 in the most common morphea subtype - MEP.
Insights
Transforming growth factor-beta 1 (TGF-β1) does not appear to play a significant role in plaque morphea. This study found no differences in TGF-β1 levels in skin, blood cells, or plasma of patients compared to healthy controls.
Area of Science:
- Dermatology
- Immunology
- Fibrosis Research
Background:
- Morphea, a rare localized scleroderma, involves skin fibrosis with unknown causes.
- Transforming growth factor-beta (TGF-β), a known profibrotic factor, has an unclear role in morphea pathogenesis.
Purpose of the Study:
- To quantify TGF-β1 expression in skin and peripheral blood mononuclear cells (PBMC).
- To measure plasma levels of TGF-β1 in plaque morphea (MEP) patients.
- To investigate the potential involvement of TGF-β1 in MEP pathogenesis.
Main Methods:
- Quantified TGF-β1 plasma levels using ELISA in 20 MEP patients and 36 controls.
- Assessed TGF-β1 expression in PBMC and skin biopsies from MEP patients and 47 and 13 healthy controls, respectively, using real-time PCR.
- Compared TGF-β1 levels between MEP patients and healthy controls, considering disease activity and duration.
Main Results:
- No significant differences in TGF-β1 expression were detected in PBMC between MEP patients and healthy controls.
- TGF-β1 levels in skin biopsies did not differ between MEP patients and controls.
- Plasma TGF-β1 levels showed no significant variation between MEP patients and healthy individuals, irrespective of disease status.
Conclusions:
- The study findings do not support a substantial role for TGF-β1 in plaque morphea, the most prevalent subtype.
- These results challenge previous claims regarding TGF-β1's involvement in morphea.
- Further research may be needed to explore other fibrotic pathways in morphea.
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