Project description:The present study was aimed to identify aberrantly expressed lncRNAs involved in the progression of SjS and explore their potential functions. Labial salivary gland of 4 SjS patients and 4 healthy controls was collected. LncRNA expression profile in labial salivary gland was analyzed by LncRNA microarray.
Project description:Differential gene expression in the salivary gland during development and onset of xerostomia in Sjögren’s syndrome-like disease of the C57BL/6.NOD-Aec1Aec2 mouse. Recently, we reported the development of the C57BL/6.NOD-Aec1Aec2 mouse that carries two genetic intervals derived from the NOD mouse capable of conferring Sjögren’s syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice. In an attempt to define the molecular bases underlying onset of stomatitis sicca (xerostomia) in this C57BL/6.NOD-Aec1Aec2 mouse model, we have carried out a study utilizing microarray technology.
Project description:To study the difference of gene expression profile in minor salivary glands of female patients with primary Sjögren’s syndrome (pSS) and healthy volunteers
Project description:The C57BL/6.NOD-Aec1Aec2 mouse is a model for primary Sjögren’s syndrome and was constructed by introducing two genetic intervals derived from the NOD mouse that confers Sjögren’s syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice. To define the chronological interrelationships of biological themes associated with progression from pre- to sub-clinical to overt spontaneous experimental SjS-like disease involving the extracellular milieu (EM) of the salivary glands, we carried out a study utilizing microarray technology in which the parental C57BL/6J mouse was used as the healthy control strain. A bioinformatics-based data analysis methodology designed for comprehensive visualization of global datasets between C57BL/6J and C57BL/6.NOD-Aec1Aec2 mice has permitted a definition of the molecular changes that correlate with onset of stomatitis sicca (xerostomia) in the SjS-susceptible mice. The transcriptome data set of C57BL/6J permitted identification of normal physiological activity.
Project description:In this study we have explored the effects of ERdj5 chaperone protein deletion in the proteome of 129SV mouse submandibular salivary glands. This knockout mouse model recapitulates many aspects of Sjögren’s Syndrome, including salivary gland inflammatory infiltrations, anti-nuclear autoantibodies and others (Apostolou et al., Front.Immunol.2019;10,506). Additionally, for 12SV wildtype animals we explore the proteome profile of the extensive sexual dimorphism observed in the submanidular glands of mice.
Project description:Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease with complex etiopathogenesis. Here we use Affymetrix U133 plus 2.0 microarray gene expression data from human parotid tissue. Parotid gland tissues were harvested from 17 pSS and 14 14 non-pSS sicca patients and 18 controls. The data were used in the following article: Nazmul-Hossain ANM, Pollard RPE, Kroese FGM, Vissink A, Kallenberg CGM, Spijkervet FKL, Bootsma H, Michie SA, Gorr SU, Peck AB, Cai C, Zhou H, Horvath S, Wong DTW (2012) Systems Analysis of Primary Sjögren’s Syndrome Pathogenesis in Salivary Glands: Comparative Pathways and Molecular Events in Humans and a Mouse Model. Parotid gland tissues were harvested from 17 pSS and 14 non-pSS sicca patients and 18 controls.
Project description:Primary Sjögren’s syndrome (pSS) is a chronic systemic autoimmune disease characterized by typical autoantibody production and lymphocytic-mediated exocrine gland damage. Interstitial lung disease (ILD) is a common complication of pSS and can be associated with a poor prognosis. However, the pathogenesis of ILD in pSS is still unclear. In this study, we used RNA sequencing to investigate the gene-expression profile of the minor salivary glands (MSGs) from 36 patients with ILD-pSS and 128 patients with non-ILD-pSS. In the remarkably enriched chemokine-mediated signaling pathway, CXCR2 was found to be significantly elevated in both MSG and plasma from pSS patients with versus without ILD (p < 0.001). Furthermore, the CXCR2 expression level in MSG and plasma was significantly associated with the diffusing capacity of the lungs for carbon monoxide, erythrocyte sedimentation rate, and EULAR Sjögren’s Syndrome Disease Activity Index in ILD-pSS. Therefore, with its potential role in ILD progression in patients with pSS and its strong association with clinical manifestations of the disease, CXCR2 may serve as a useful index for disease activity in ILD associated with pSS.
Project description:Differential gene expression in the salivary gland during development and onset of xerostomia in SjM-CM-6grenM-bM-^@M-^Ys syndrome-like disease of the C57BL/6.NOD-Aec1Aec2 mouse. Recently, we reported the development of the C57BL/6.NOD-Aec1Aec2 mouse that carries two genetic intervals derived from the NOD mouse capable of conferring SjM-CM-6grenM-bM-^@M-^Ys syndrome (SjS)-like disease in SjS-non-susceptible C57BL/6 mice. In an attempt to define the molecular bases underlying onset of stomatitis sicca (xerostomia) in this C57BL/6.NOD-Aec1Aec2 mouse model, we have carried out a study utilizing microarray technology. The present study was designed to define the changing gene expression profiles within the salivary glands of C57BL/6.NOD-Aec1Aec2 mice at five time points representing a pre-disease stage (4 weeks), the early pre-clinical stage (8 weeks), the initial influx of leukocytes into the salivary glands (12 weeks), the early clinical phase of autoimmunity (16 weeks), and the early onset of clinical SjSlike disease characterized by secretory dysfunction (20 weeks). The C57BL/6.NOD-Aec1Aec2 mouse is a model of primary SjS in which the Idd3 region of chromosome 3 and the Idd5 region of chromosome 1 derived from the NOD mouse were bred into the non-autoimmune C57BL/6 mouse, resulting in a SjS-like disease susceptibility that mimics both the pathophysiological characteristics and reduced secretory responses observed with NOD mice during development and onset of disease. This SjS-susceptible strain was designated C57BL/6.NOD-Aec1Aec2, where Aec1 corresponds to Idd3 (of chromosome 3) and Aec2 corresponds to Idd5 (of chromosome 1).
