Bcl-2 family expression in salivary glands from patients with primary Sjogren's syndrome: Involvement of Bax in salivary gland destruction

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

Bcl-2 family expression in salivary glands from patients with primary Sjogren's syndrome: Involvement of Bax in salivary gland destruction

Liping Kong, Noriyoshi Ogawa, H. Stan McGuff, Toru Nakabayashi, Ken Mei Sakata, Reiji Masago, Norma Vela-Roch, Norman Talal, Howard Dang

Research output: Contribution to journal › Article › peer-review

57 Scopus citations

Abstract

To investigate the molecular mechanism of glandular parenchyma destruction in Sjogren'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 by in situ 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.

Original language	English (US)
Pages (from-to)	133-141
Number of pages	9
Journal	Clinical Immunology and Immunopathology
Volume	88
Issue number	2
DOIs	https://doi.org/10.1006/clin.1998.4556
State	Published - Aug 1998

Keywords

Apoptosis
Bcl-2
Salivary glands
Sjogren's syndrome

ASJC Scopus subject areas

Immunology and Allergy
Pathology and Forensic Medicine
Immunology

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Bcl-2 family expression in salivary glands from patients with primary Sjogren's syndrome : Involvement of Bax in salivary gland destruction. / Kong, Liping; Ogawa, Noriyoshi; McGuff, H. Stan; Nakabayashi, Toru; Sakata, Ken Mei; Masago, Reiji; Vela-Roch, Norma; Talal, Norman; Dang, Howard.

In: Clinical Immunology and Immunopathology, Vol. 88, No. 2, 08.1998, p. 133-141.

Research output: Contribution to journal › Article › peer-review

Kong, Liping ; Ogawa, Noriyoshi ; McGuff, H. Stan ; Nakabayashi, Toru ; Sakata, Ken Mei ; Masago, Reiji ; Vela-Roch, Norma ; Talal, Norman ; Dang, Howard. / Bcl-2 family expression in salivary glands from patients with primary Sjogren's syndrome : Involvement of Bax in salivary gland destruction. In: Clinical Immunology and Immunopathology. 1998 ; Vol. 88, No. 2. pp. 133-141.

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title = "Bcl-2 family expression in salivary glands from patients with primary Sjogren's syndrome: Involvement of Bax in salivary gland destruction",

abstract = "To investigate the molecular mechanism of glandular parenchyma destruction in Sjogren'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 by in situ 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.",

keywords = "Apoptosis, Bcl-2, Salivary glands, Sjogren's syndrome",

author = "Liping Kong and Noriyoshi Ogawa and McGuff, {H. Stan} and Toru Nakabayashi and Sakata, {Ken Mei} and Reiji Masago and Norma Vela-Roch and Norman Talal and Howard Dang",

note = "Funding Information: The authors are grateful to Karen Aufdemorte for preparing the tissue sections. This research was supported by U.S. Public Health Service Grants (NIH) DE 09311 and DE 10863 and the RGK Foundation (Austin, TX). Dr. Ogawa is a recipient of a Sj{\"o}gren{\textquoteright}s Syndrome Foundation Fellowship (Jericho, NY).",

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N2 - To investigate the molecular mechanism of glandular parenchyma destruction in Sjogren'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 by in situ 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.

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