X-linked ectodermal dysplasia receptor (XEDAR) gene silencing prevents caspase-3-mediated apoptosis in Sjögren’s syndrome

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• 作者：Margherita Sisto ; Loredana Lorusso ; Sabrina Lisi
• 关键词：Sjögren’s syndrome ; Ectodysplasin ; A2 ; XEDAR ; Apoptosis ; Caspase ; 3
• 刊名：Clinical and Experimental Medicine
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：17
• 期：1
• 页码：111-119
• 全文大小：
• 刊物主题：Internal Medicine; Hematology; Oncology;
• 出版者：Springer International Publishing
• ISSN：1591-9528
• 卷排序：17

文摘

Despite recent advancements in the knowledge of the etiology and pathogenic mechanisms, treatment of the autoimmune disease Sjögren’s syndrome (SS) remains mostly empiric and symptom-based, indicating the need for novel therapeutic approaches. Ectodysplasin-A2 (EDA-A2) is a recently isolated member of the tumor necrosis factor superfamily that binds to X-linked ectodermal dysplasia receptor (XEDAR). In this report, we have analyzed the expression and the biological activity of EDA-A2 in human salivary gland epithelial cells (SGEC) from primary Sjögren’s syndrome (pSS) patients. We report that EDA-A2 and its receptor XEDAR are overexpressed in pSS SGEC in comparison with healthy individuals and that the EDA-A2/XEDAR system in these cells is involved in the induction of apoptosis via caspases activation. Collectively, our results suggest that EDA-A2/XEDAR system may be a promising agent for the gene therapy of pSS.