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Comparison of the tissue expressions of glutathione S transferase isoenzymes among patients with morphea and healthy controls: A preliminary study
Author(s) -
Uzuncakmak Tugba Kevser,
Koska Mahmut Can,
Ozkanli Seyma,
Kaya Kocdogan Arzu,
Oguztuzun Serpil,
Karadag Ayse Serap,
Akdeniz Necmettin,
Wollina Uwe
Publication year - 2020
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1111/dth.14363
Subject(s) - morphea , medicine , gstp1 , pathology , glutathione s transferase , pathogenesis , connective tissue , biopsy , isozyme , skin biopsy , oxidative stress , connective tissue disease , glutathione , enzyme , biology , autoimmune disease , disease , biochemistry
Morphea is an inflammatory connective tissue disorder, which is characterized by sclerosis in skin and subcutaneous tissues with a chronic progress. The oxidative stress in pathogenesis of sclerosing diseases was proposed in several studies with conflicting results. To explore the tissue expressions of Glutathione S transferase (GST) isoenzymes in patients with morphea and compare these expressions with healthy controls. Twenty‐two morphea patients and 20 sex and age matched healthy controls were enrolled in this study. Four millimeter punch biopsies were performed from the active sclerotic plaques of morphea patients. Tissue samples of control group were obtained from nonlesional normal skin biopsy specimens. The protein expressions of GST isoenzymes were analyzed immunohistochemically. Tissue expressions of GSTP1, GSTT1, and GSTA1 isoenzymes in morphea patients were found to be significantly higher than in control tissues. There was no significant difference in GSTM1 isoenzyme expression between the two groups. The increased tissue expressions of GSTA1, GSTP1, and GSTT1 isoenzymes in morphea may represent the activated GST enzymes in response to excessive free radical formation and may also support the hypothesis of increased oxidative stress in morphea etiopathogenesis.