Mus musculus
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ABSTRACT:
PROVIDER: PRJNA115643 | ENA |
REPOSITORIES: ENA
Similar Datasets
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.
2009-04-11 | GSE15640 | GEO
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).
2009-04-11 | E-GEOD-15640 | biostudies-arrayexpress
Project description:Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease that is estimated to affect 35 million people worldwide. Currently, no effective treatments exist for Sjögren’s syndrome, and there is a limited understanding of the physiological mechanisms associated with xerostomia and hyposalivation. The present work revealed that aquaporin 5 expression, a water channel critical for salivary gland fluid secretion, is regulated by bone morphogenetic protein 6. In- creased expression of this cytokine is strongly associated with the most common symptom of primary Sjögren’s syndrome, the loss of salivary gland function. This finding led us to develop a novel ther- apy in the treatment of Sjögren’s syndrome by increasing the water permeability of the gland to restore saliva flow. Our study demon- strates that the targeted increase of gland permeability not only resulted in the restoration of secretory gland function but also re- solved the hallmark salivary gland inflammation and systemic inflam- mation associated with disease. Secretory function also increased in the lacrimal gland, suggesting this local therapy could treat the sys- temic symptoms associated with primary Sjögren’s syndrome.
2016-07-20 | GSE80225 | GEO
Project description:Genome wide DNA methylation profiling of human labial salivary gland (LSG) biopsy samples obtained from 28 female members of the Sjögren's International Collaborative Clinical Alliance (SICCA) Registry. The Illumina HumanMethylation450 BeadChip platform was used to obtain DNA methylation profiles across more than 450,000 highly informative CpG sites. Samples included 15 non-case glands, and 13 glands from patients with Sjögren's Syndrome.
2018-02-02 | GSE110007 | GEO
Project description:Salivary gland hypofunction is a common adverse effect during and after radiotherapy of head and neck cancers, resulting in the dry mouth syndrome called xerostomia. Previous studies suggested that the functionality of the salivary gland is under the regulation of the circadian clock, however, the extent and scope of this regulation remains unexplored. Here, we profiled the diurnal fluctuation of gene expression in the mouse submandibular salivary gland. We further analyzed the regulatory role of key circadian transcription factors Bmal1, Nr1d1 (Rev-erba), and Dbp, which revealed a wide range of potential down-stream target genes. The circadian clock was disrupted upon irradiation, as revealed by gene expression analysis. We propose that the mechanism of salivary gland hypofunction in radiotherapy involves perturbation of the circadian clock.
2024-01-01 | GSE234789 | GEO
Project description:Ionizing radiation (IR) – induced salivary gland damage is a common adverse effect in radiotherapy for patients with head and neck cancers. Currently, there is no effective treatment for the resulting salivary gland hypofunction and xerostomia (dry mouth). Here we profiled the acute gene expression change in the mouse submandibular salivary gland, and defined its damage response patterns at the transcriptome level.
2021-09-23 | GSE184673 | GEO
Project description:Primary Sjogren’s syndrome (pSS) is an autoimmune disease characterized by xerostomia (dry mouth), lymphocytic infiltration into salivary glands and the presence of SSA and SSB autoantibodies. Xerostomia is caused by hypofunction of the salivary glands and has been considered a driver in pSS development. Saliva production is regulated by sympathetic input into the gland initiating intracellular Ca2+ signals that activate the store operated Ca2+ entry (SOCE) pathway eliciting sustained Ca2+ influx. SOCE is mediated by the STIM1 and STIM2 proteins and the ORAI1 Ca2+ channel. However, there are no studies on the effects of lack of STIM1/2 function in salivary acini in animal models or its impact on pSS. Here we report that male and female mice lacking Stim1 and Stim2 (Stim1/2K14Cre) in salivary glands hyposalivate upon pilocarpine stimulation and showed reduced intracellular Ca2+ levels via SOCE in parotid acini. Bulk RNASeq of the parotid glands of Stim1/2K14Cre showed a decrease in Stim1/2 genes but not in other Ca2+ associated genes mediating saliva fluid secretion, yet SOCE was functionally required for the activation of the Ca2+ activated chloride channel ANO1. Ageing Stim1/2K14Cre mice showed no evidence of lymphocytic infiltration in the glands or elevated levels of SSA or SSB autoantibodies in the serum which may be linked to the downregulation of the toll-like receptor 8 (Tlr8) in Stim1/2K14Cre mice. This is supported by an increase in TLR8 gene expression in a salivary gland cell line following SOCE stimulation. Moreover, salivary gland biopsies of pSS patients showed increased STIM1 and TLR8 expression. These results implicate SOCE as an important activator of ANO1 and saliva fluid secretion in salivary glands but loss of SOCE does not result in pSS. Importantly, our data suggest a link between SOCE and TLR8 signaling which may have implications in inflammatory responses in salivary glands.
2025-02-19 | GSE251691 | GEO
Project description:Epigenetic Signatures of Salivary Gland Inflammation in Sjögren's Syndrome.
| PRJNA432548 | ENA
Project description:The C57BL/6.NOD-Aec1Aec2 mouse is a model for primary SjM-CM-6grenM-bM-^@M-^Ys syndrome and was constructed by introducing two genetic intervals derived from the NOD mouse that confers SjM-CM-6grenM-bM-^@M-^Ys 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. The study was designed to define the changing gene expression profiles within the salivary glands of C57BL/6.NOD-Aec1Aec2 mice at multiple 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), and the early clinical phase of autoimmunity (16 weeks) to characterize the influence of the extracellular milieu on early development of disease. Because the C57BL/6.NOD-Aec1Aec2 mouse was derived from the C57BL/6J line, C57BL/6J mice were used as the comparative healthy controls. This comparison permitted the identification of disease-associated gene expressions by subtracting out normal physiological processes. This present study represents the C57BL/6J healthy control mice. Series GSE15640 includes the data for the C57BL/6.NOD-Aec1Aec2 mice.
2012-03-10 | E-GEOD-36378 | biostudies-arrayexpress
Project description: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 genomic microarray technology.
2013-06-25 | GSE48139 | GEO