Liping Kong , Noriyoshi Ogawa , H.Stan McGuff , Toru Nakabayashi , Ken-mei Sakata , Reiji Masago , Norma Vela-Roch , Norman Talal , Howard Dang
{"title":"Bcl-2 Family Expression in Salivary Glands from Patients with Primary Sjögren's Syndrome: Involvement of Bax in Salivary Gland Destruction","authors":"Liping Kong , Noriyoshi Ogawa , H.Stan McGuff , Toru Nakabayashi , Ken-mei Sakata , Reiji Masago , Norma Vela-Roch , Norman Talal , Howard Dang","doi":"10.1006/clin.1998.4556","DOIUrl":null,"url":null,"abstract":"<div><p>To investigate the molecular mechanism of glandular parenchyma destruction in Sjögren's syndrome (SS), Bcl-2, Bax, Bcl-X, and Bak expression were studied. SS (<em>n</em>= 18) and control salivary glands (<em>n</em>= 6) were examined by immunohistochemistry. Apoptosis was assessed by<em>in situ</em>DNA nick end labeling. Infiltrating mononuclear cells in the SS salivary gland showed elevated Bcl-2. These mononuclear cells expressed increased Bax but did not undergo apoptosis. Both SS and control salivary gland ductal epithelial cells expressed Bcl-2, Bax, and Bcl-X. SS, but not normal, salivary gland acinar cells expressed Bax and underwent apoptosis. These results suggest that elevated Bax expression in SS salivary gland acinar cells may play an important role in the apoptotic pathway. In contrast, Bcl-2 expression in SS infiltrating mononuclear cells and ductal cells may contribute to their survival.</p></div>","PeriodicalId":10683,"journal":{"name":"Clinical immunology and immunopathology","volume":"88 2","pages":"Pages 133-141"},"PeriodicalIF":0.0000,"publicationDate":"1998-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/clin.1998.4556","citationCount":"77","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical immunology and immunopathology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0090122998945561","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 77
Abstract
To investigate the molecular mechanism of glandular parenchyma destruction in Sjögren's syndrome (SS), Bcl-2, Bax, Bcl-X, and Bak expression were studied. SS (n= 18) and control salivary glands (n= 6) were examined by immunohistochemistry. Apoptosis was assessed byin situDNA nick end labeling. Infiltrating mononuclear cells in the SS salivary gland showed elevated Bcl-2. These mononuclear cells expressed increased Bax but did not undergo apoptosis. Both SS and control salivary gland ductal epithelial cells expressed Bcl-2, Bax, and Bcl-X. SS, but not normal, salivary gland acinar cells expressed Bax and underwent apoptosis. These results suggest that elevated Bax expression in SS salivary gland acinar cells may play an important role in the apoptotic pathway. In contrast, Bcl-2 expression in SS infiltrating mononuclear cells and ductal cells may contribute to their survival.