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A potential contribution of decreased galectin‐7 expression in stratified epithelia to the development of cutaneous and oesophageal manifestations in systemic sclerosis
Author(s) -
Saigusa Ryosuke,
Yamashita Takashi,
Miura Shunsuke,
Hirabayashi Megumi,
Nakamura Kouki,
Miyagawa Takuya,
Fukui Yuki,
Yoshizaki Ayumi,
Sato Shinichi,
Asano Yoshihide
Publication year - 2019
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13900
Subject(s) - medicine , immunostaining , endothelin 1 , galectin , stimulation , endocrinology , immunohistochemistry , galectin 3 , epidermis (zoology) , autocrine signalling , fibrosis , pathology , biology , immunology , receptor , anatomy
Backgrounds Stratified epithelia have caught much attention as potential contributors to the development of dermal and oesophageal fibrosis in systemic sclerosis ( SS c). Galectin‐7 is a marker of all types of stratified epithelia, which is involved in the maintenance of epidermal homeostasis. So far, the role of galectin‐7 has not been studied in SS c. Objectives To investigate the potential contribution of galectin‐7 to the development of clinical manifestations in SS c. Methods Galectin‐7 expression was examined in skin samples and cultured keratinocytes by immunostaining and/or quantitative reverse transcription PCR . Serum galectin‐7 levels were determined by enzyme‐linked immunosorbent assay in 63 SS c and 20 healthy subjects. Results Galectin‐7 expression was markedly decreased in the epidermis of SS c lesional skin compared with that of healthy control skin. Serum galectin‐7 levels were significantly lower in SS c patients than in healthy controls and inversely correlated with skin score. In addition, SS c patients with diffuse pigmentation and those with oesophageal dysfunction had significantly decreased serum galectin‐7 levels as compared to those without each symptom. Importantly, endothelin‐1 stimulation suppressed galectin‐7 expression in normal human keratinocytes, and bosentan, a dual endothelin receptor antagonist, reversed circulating galectin‐7 levels and epidermal galectin‐7 expression in SS c patients. Conclusions Galectin‐7 downregulation in stratified epithelia, which is mediated at least partially by autocrine endothelin stimulation, may contribute to the development of cutaneous manifestations and oesophageal dysfunction in SS c patients.