Ozkay Ozgor, Gulsen Akoglu, Nuran Sungu, Eda Karaismailoglu, Akin Aktas
Indian Journal of Dermatology, Venereology, and Leprology 2017 83(5):556-560
Background: Enhanced expression and excitation of the receptor for advanced glycation end products is considered to play a role in the regulation of many pro-inflammatory genes involved in the pathogenesis of psoriasis. Aim: We investigated the expression of receptor for advanced glycation end product in various cell types, in lesional and peri-lesional skin of patients with psoriasis, and its correlation with disease severity. Methods: Paraffin-embedded punch biopsy tissue taken from psoriatic plaques and peri-lesional normal appearing skin tissue of twenty patients with psoriasis, and normal skin samples of eleven healthy participants, were enrolled in the study. The sections were stained immunohistochemically with anti-receptor for advanced glycation end product antibody. The intensity of receptor for advanced glycation end product expression was assessed semi-quantitatively on epidermal cells, microvascular endothelium, dermal fibroblasts and inflammatory cells. They were graded as follows: 0 (no staining), 1 (weak), 2 (moderate) and 3 (strong) intensity. Results: Receptor for advanced glycation end product expression on epidermis, microvascular endothelium, inflammatory cells and fibroblasts in the psoriatic plaques was more intense than perilesional and normal tissue (all P < 0.05). It did not correlate with disease severity. Limitations: The main limitation of our study is that this was a semi-quantitative assessment, detected immunohistochemically in skin biopsies. Conclusion: Receptor for advanced glycation end product expression may have an important role in psoriasis pathogenesis, independent of disease severity.
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Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,alsfakia@gmail.com,
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Publication date: January–February 2018 Source: Materials Today, Volume 21, Issue 1 Author(s): David Bradley http://ift.tt/2BP...
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