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Transforming growth factor-?1 in plaque morphea.

ABSTRACT: INTRODUCTION:Morphea (localized scleroderma) is a rare cutaneous disease characterized by skin fibrosis of unknown pathogenesis. Transforming growth factor-? (TGF-?) is a potent profibrotic factor. The role of TGF-? in morphea remains unclear. AIM:The goal of this study was to estimate the expression level of TGF-?1 in skin and peripheral blood mononuclear cells as well as the plasma levels of TGF-?1 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-?1 plasma levels was performed with the use an adequate ELISA kit, while real-time polymerase chain reaction was employed for the expression of TGF-?1 in peripheral blood mononuclear cells (PBMC) and skin. RESULTS:In our study we have not detected differences in TGF-? 1 expression in PBMC, skin, nor in plasma levels of TGF-?1 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-?1 in the most common morphea subtype - MEP.

SUBMITTER: Danczak-Pazdrowska A

PROVIDER: S-EPMC3907897 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

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Transforming growth factor-β1 in plaque morphea.

Dańczak-Pazdrowska Aleksandra A Kowalczyk Michał J MJ Szramka-Pawlak Beata B Gornowicz-Porowska Justyna J Szewczyk Aleksandra A Silny Wojciech W Molińska-Glura Marta M Olewicz-Gawlik Anna A Zaba Ryszard R Pazdrowski Jakub J Hrycaj Paweł P

Postepy dermatologii i alergologii 20131218 6

<h4>Introduction</h4>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.<h4>Aim</h4>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).<h4>Material and methods</h4>The study involved 20 MEP pa ...[more]

PMID: 24493995

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Project description:BackgroundNerve growth factor (NGF) contributes to pain in knee osteoarthritis (KOA) patients. Transforming growth factor-beta (TGF-β) stimulates NGF expression in chondrocytes from KOA patients. However, the correlation between synovial TGF-β and NGF levels has not been sufficiently studied in human KOA patients. Further, the mechanism governing NGF regulation by TGF-β in synovial cells is unclear.MethodsDuring total knee arthroplasty, we extracted the synovial tissue (SYT) of 107 subjects with unilateral Kellgren/Lawrence grade 3-4 KOA confirmed by radiography. We examined the distribution of TGF-β and NGF using immunohistochemistry, and analyzed the relationship between NGF and TGFB mRNA levels. Cultured synovial cells extracted from SYT were exposed to culture medium (control), human recombinant TGF-β (rhTGF-β), rhTGF-β + ALK5 inhibitor SB505124, rhTGF-β + transforming growth factor activating kinase 1 (TAK1) inhibitor (5Z)-7-oxozeaenol, or rhTGF-β + p38 inhibitor SB203580 for 30 min, 6 h and 24 h. NGF mRNA expressed by the cultured cells and NGF protein levels in the cell supernatant were detected by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Phosphorylation of p38 was evaluated by western blotting.ResultsNGF mRNA levels were positively correlated with those of TGFB. Cells expressing TGF-β and NGF protein were observed in the lining layer of SYT. TGF-β stimulated increased NGF mRNA expression and NGF protein production. The ALK5 inhibitor completely suppressed the TGF-β-mediated increase in NGF expression and NGF production in synovial cells. ALK5, TAK1 and p38 inhibitors inhibited the TGF-β-induced phosphorylation of p38, and TAK1 and p38 inhibitors partially inhibited the TGF-β-mediated increase in NGF expression and NGF production in synovial cells.ConclusionTGF-β regulates NGF production via the TGF-β/ALK5 signaling pathway in osteoarthritic synovium. This effect may partially occur through inhibition of the TAK1/p38 pathway in the SYT of KOA patients.

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Transforming growth factor-?1 in plaque morphea.

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Transforming growth factor-β1 in plaque morphea.

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