Evidence map›Paper›PMID 38912838›Full record

ArticleClinical and experimental immunology2024

Beta-adrenergic stimulation promotes an endoplasmic reticulum stress-dependent inflammatory program in salivary gland epithelial cells.

Kalliopi Moustaka, Athanasios Stergiopoulos, Roxane Tenta, Sophia Havaki, Stergios Katsiougiannis, Fotini N Skopouli

Abstract read
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In one paragraph

Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Kalliopi MoustakaDepartment of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.ORCID 0009-0008-0037-4172
Athanasios StergiopoulosDepartment of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.ORCID 0000-0002-7908-0669
Roxane TentaDepartment of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.ORCID 0000-0002-4867-6945
Sophia HavakiDepartment of Histology and Embryology, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Stergios KatsiougiannisDepartment of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.ORCID 0000-0002-2475-4638
Fotini N SkopouliDepartment of Nutrition and Dietetics, School of Health Science and Education, Harokopio University, Athens, Greece.

Funding

H2020 project HARMONICSS 731944
6 · The paper itself

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 β-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 β-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 β-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.

Indexed as

Activating Transcription Factor 4eIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEpinephrineEpithelial CellsInterleukin-6Salivary GlandsTaurochenodeoxycholic AcidAdrenergic beta-AgonistsCells, CulturedCyclic AMPFemaleHumansInflammationReceptors, Adrenergic, betaActivating Transcription Factor 4Adrenergic beta-AgonistsATF4 protein, humanCyclic AMPEIF2AK3 protein, humaneIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEpinephrineHSPA5 protein, humanIL6 protein, humanInterleukin-6Receptors, Adrenergic, betaTaurochenodeoxycholic Acidursodoxicoltaurineendoplasmic reticulum stressinterleukin-6PERK/ATF4 pathwaysalivary gland epithelial cellsSjögren’s syndromeβ-adrenergic stimulation

Identifiers

PMID38912838
PMCPMC11404117

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.