Haiyan Yu, Ulrich Mrowietz, Oliver Seifert
DOI: 10.2340/00015555-0634

Transforming growth factor beta (TGFβ) has been suggested to be an effective inhibitor of the increased keratinocyte proliferation in psoriasis. Three TGFβ isoforms are described (TGFβ1, 2 and 3), signalling via a heteromeric receptor complex of TGFβRI and TGFβRII. Receptor binding activates SMAD2, 3 and 4, which translocate into the nucleus and regulate TGFβ-responsive genes. SMAD6 and 7 proteins represent a negative feedback loop inhibiting the TGFβ-SMAD signalling path­way. As TGFβ1 overexpression inhibits keratinocyte proliferation, the aim of this study was to investigate with real-time RT-PCR the expression of TGFβ1, 2 and 3, TGFβRI and TGFβRII and SMAD2, 3, 4, 6 and 7 in lesional and non-lesional psoriatic skin from 13 patients with chronic plaque-type psoriasis as compared to skin from 10 healthy subjects . The study data demonstrate significantly downregulated TGFβRI and SMAD2, 4 and 6 mRNA expression in lesional and non-lesional psoriatic skin. SMAD7 mRNA expression was significantly decreased in lesional psoriatic skin compared with both non-lesional psoriatic skin and healthy skin. A significant TGFβ3 and TGFβRII mRNA upregulation exclusively in non-lesional psoriatic skin but no significant difference in the expression of TGFβ1 and 2 was found. The results of this study suggest that the expression of TGFβ isoforms, receptors and SMADs may be involved in the increased proliferation of keratinocytes in psoriatic skin.