科研之友
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摘要
Transforming growth factor beta (TGF beta) has been suggested to be an effective inhibitor of the increased keratinocyte proliferation in psoriasis. Three TGF beta isoforms are described (TGF beta 1, 2 and 3), signalling via a heteromeric receptor complex of TGF beta RI and TGF beta RII. Receptor binding activates SMAD2, 3 and 4, which translocate into the nucleus and regulate TGF beta-responsive genes. SMAD6 and 7 proteins represent a negative feedback loop inhibiting the TGF beta-SMAD signalling pathway. As TGF beta 1 overexpression inhibits keratinocyte proliferation, the aim of this study was to investigate with real-time RT-PCR the expression of TGF beta 1, 2 and 3, TGF beta RI and TGF beta RII 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 TGF beta RI 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 TGF beta 3 and TGF beta RII mRNA upregulation exclusively in non-lesional psoriatic skin but no significant difference in the expression of TGF beta 1 and 2 was found. The results of this study suggest that the expression of TGF beta isoforms, receptors and SMADs may be involved in the increased proliferation of keratinocytes in psoriatic skin.
- 出版日期2009
- 单位浙江大学
