Dataset Information

Salivary Protein Biomarker Detection of Saliva Secretion Disorder in a Primary Sjögren Syndrome Murine Model

ABSTRACT: Decreased salivary flow is one of the most common symptoms in primary Sjögren syndrome (pSS). The present study was designed to identify a salivary protein biomarker related to saliva secretion disorder in NOD/ShiLtJ mice, a pSS primary murine model. The stimulated saliva was collected from NOD/ShiLtJ and BALB/c mice as controls for differential proteomic analysis.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Saliva

SUBMITTER: Qian Tao

LAB HEAD: Qian Tao

PROVIDER: PXD008199 | Pride | 2018-03-21

REPOSITORIES: Pride

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Publications

Detection of salivary protein biomarkers of saliva secretion disorder in a primary Sjögren syndrome murine model.

Liang Peisheng P Zhu Wangyong W Lan Tianjun T Tao Qian Q

Journal of pharmaceutical and biomedical analysis 20180312

Saliva secretion disorder is one of the most common symptoms in primary Sjögren syndrome (pSS). Salivary biomarkers related to saliva secretion disorder were identified in a pSS murine model, NOD/ShiLtJ mouse, using differential proteomic analysis. Candidate biomarkers were screened with Kyoto Encyclopedia of Genes and Genomes pathway analysis and validated in saliva and salivary glands by western blotting and immunohistochemistry (IHC). Biological functions were detected using ingenuity pathway ...[more]

PMID: 29558726

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Project description:In order to understand how biochemical and genetic differences correlate with treatment response, we measured depressive-like behavior, gene expression and the levels of thirty-six neurobiochemical analytes across a panel of genetically-diverse mouse inbred lines after chronic treatment with vehicle or fluoxetine. Neurobiochemical markers were chosen based on their putative molecular function within pathways proposed to underlie depression, which include neuronal transmission, HPA-axis regulation, and neuroimmune processes. The goal of this study is to establish genetic and biochemical biomarkers that can predict treatment response and to propose a molecular pathway that is critical in mediating anti-depressant response. Thirty mouse inbred strains (129S1/SvImJ, A/J, AKR/J, BALB/cJ, BTBRT T(+) tf/J, BUB/BnJ, C3H/HeJ, C57BL/6J, C57BLKS/J, C57BR/cdJ, C58/J, CBA/J, CE/J, DBA/2J, FVB/NJ, I/LnJ, LG/J, LP/J, MA/MyJ, MRL/MpJ, NOD/LtJ, NOR/LtJ, NZB/BlNJ, NZW/LacJ, P/J, PL/J, RIIIS/J, SJL/J, SM/J, and SWR/J) aged 5-6 weeks old were obtained from The Jackson Laboratory (Bar Harbor, ME). Male mice were kept in polycarbonate cages on a 12-hour light/dark cycle (lights on at 0700h) with access to food and water ad libitum. Following one week of habituation, mice were randomized to either control or treatment group (n=12 male mice per strain per treatment group). Mean water intake for each strain was determined previously by measuring daily water consumption for three weeks (n=12 mice per strain). This information, along with average weight measurements for each strain, was used to determine the amount of fluoxetine required to provide a daily oral dose of 0 or 18 mg/kg per mouse. After chronic administration of 0 or 18 mg/kg of fluoxetine for 21 days, mice aged 9-10 weeks were tested in a tail-suspension and open field apparatus. Upon completion of the study, mice were sacrificed by cervical dislocation and decapitation between 0900h and 1300h. Trunk blood was quickly collected and allowed to clot on ice. Following centrifugation, serum samples were collected and stored at -20C for determination of fluoxetine and norfluoxetine levels using liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS). Micro-dissections of individual regions were performed on serial coronal brain sections (approximately 10 µm) that were placed on a cold metal block. Cortex was taken from the same section for each animal and immediately snaps frozen on dry ice. Samples were stored at -80C until analysis.

Project description:Aims/hypothesis AGEs are considered environmental contributors of type 1 diabetes, but the exact role AGEs play early in pathogenesis of the disease, remains unidentified. We aimed to reduce AGEs with the pharmacotherapy alagebrium chloride in MIN6N8 cells and early in life in NOD mice to determine its impact on beta cell immunogenicity, function, and disease progression. Methods MIN6N8 cells were cultured with AGEs with or without short-term alagebrium therapy to determine the effect on ER stress and beta cell antigen presentation via a reporter assay for protein responses in the unfolded protein response, the enzymatic activity of endoplasmic reticulum aminopeptidase-1 (ERAP1) and the immunopeptidome. To determine the effect of short-term alagebrium therapy on beta cells in vivo, female NOD mice were treated with alagebrium and insulin secretion, insulitis, and immune cell repertoire were studied. Adoptive transfer studies and diabetes progression studies were used to consider the impact of alagebrium on immune cell function and disease outcome. Results In MIN6N8 cells, alagebrium therapy inhibited the induction of endoplasmic reticulum (ER) stress and the activity of ERAP1 by AGE-modified proteins. Alagebrium treated-MIN6N8 cells did not change the MHC Class I presentation of known beta cell antigens but did induce proteomic changes related to ER homeostatic pathways. Prior to overt autoimmune diabetes, female NOD mice treated with alagebrium for 30-40 days had improved insulin secretion, reduced insulitis and amplified proportions of pancreatic CD8+ T cells, mature B cells and F4/80+ macrophages. Splenocytes from alagebrium-treated mice adoptively transferred disease to NODscid recipients and maintained interferon production in vitro. While partial protection of islets by alagebrium was seen following the adoptive transfer of activated NOD G9C8 transgenic TCR CD8+ T cells, alagebrium therapy in NOD mice did not reduce diabetes progression. Conclusions/interpretation Our data suggests that in experimental models of diabetes, short-term alagebrium treatment allows for beta cell improvement, and maintenance of immune cell function, which does not fully mitigate diabetes progression.

Dataset Information

Salivary Protein Biomarker Detection of Saliva Secretion Disorder in a Primary Sjögren Syndrome Murine Model

Publications

Detection of salivary protein biomarkers of saliva secretion disorder in a primary Sjögren syndrome murine model.

Similar Datasets

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