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Beta-adrenergic stimulation promotes an endoplasmic reticulum stress-dependent inflammatory program in salivary gland epithelial cells.
Moustaka, Kalliopi; Stergiopoulos, Athanasios; Tenta, Roxane; Havaki, Sophia; Katsiougiannis, Stergios; Skopouli, Fotini N.
Afiliación
  • Moustaka K; Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.
  • Stergiopoulos A; Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.
  • Tenta R; Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.
  • Havaki S; Department of Histology and Embryology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
  • Katsiougiannis S; Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.
  • Skopouli FN; Laboratory of Autoimmunity, Biomedical Research Foundation Academy of Athens, Athens, Greece.
Clin Exp Immunol ; 218(1): 65-74, 2024 Sep 16.
Article en En | MEDLINE | ID: mdl-38912838
ABSTRACT
The effect of beta-adrenergic stimulation on human labial minor salivary gland epithelial cells (LMSGEC) on IL-6 production and its dependency on endoplasmic reticulum (ER) stress were investigated. Primary LMSGEC from Sjögren's syndrome (SS) patients and controls in culture were stimulated with epinephrine and IL-6 expression was evaluated by qPCR and ELISA. The expression of ß-ARs in cultured LMSGEC was tested by qPCR, while adrenoceptors and cAMP levels were examined in LMSGs by immunofluorescence. ER evaluation was performed by transmission electron microscopy (TEM) and ER stress by western blot. Epinephrine-induced IL-6 production by cultured LMSGEC was evaluated after alleviation of the ER stress by applying tauroursodeoxycholic acid (TUDCA) and silencing of PKR-like ER kinase (PERK) and activating transcription factor 4 (ATF4) RNAs. Expression of IL-6 by LMSGEC was upregulated after ß-adrenergic stimulation, while the silencing of adrenoreceptors downregulated IL-6. The amelioration of ER stress, as well as the silencing of PERK/ATF4, prevented epinephrine-induced upregulation of IL-6. Adrenergic stimulation led to higher and sustained IL-6 levels secreted by LMSGEC of SS patients compared to controls. Adrenergic signaling was endogenously enhanced in LMSGEC of SS patients (expression of ß-ARs in situ, intracellular cAMP in cultured LMSGEC). In parallel, SS-LMSGEC expressed dilated ER (TEM) and higher levels of GRP78/BiP. PERK/ATF4 pathway of the ER stress emerged as a considerable mediator of adrenergic stimulation for IL-6 production by the LMSGEC. An enhanced endogenous adrenergic activation and a stressed ER observed in SS-LMSGEC may contribute to a sustained IL-6 production by these cells after adrenergic stimulation.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glándulas Salivales / Ácido Tauroquenodesoxicólico / Epinefrina / Interleucina-6 / EIF-2 Quinasa / Células Epiteliales / Factor de Transcripción Activador 4 / Estrés del Retículo Endoplásmico / Chaperón BiP del Retículo Endoplásmico Límite: Female / Humans Idioma: En Revista: Clin Exp Immunol Año: 2024 Tipo del documento: Article País de afiliación: Grecia Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glándulas Salivales / Ácido Tauroquenodesoxicólico / Epinefrina / Interleucina-6 / EIF-2 Quinasa / Células Epiteliales / Factor de Transcripción Activador 4 / Estrés del Retículo Endoplásmico / Chaperón BiP del Retículo Endoplásmico Límite: Female / Humans Idioma: En Revista: Clin Exp Immunol Año: 2024 Tipo del documento: Article País de afiliación: Grecia Pais de publicación: Reino Unido