Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-48139
PROVIDER: PRJNA209303 | 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: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
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: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.
2012-03-10 | GSE36378 | GEO
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 Sjogren'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. The present study was designed to define the changing gene expression profiles within the Lacrimal 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 Lacrimal glands (12 weeks), the early clinical phase of autoimmunity (16 weeks), and the early onset of clinical SjS-like 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).
2013-06-25 | E-GEOD-48139 | biostudies-arrayexpress
Project description:Differential gene expression in the Lacrimal gland during development and onset of xerostomia in Sjogren's syndrome-like disease of the C57BL/6.NOD-Aec1Aec2 mouse.
2015-07-15 | E-GEOD-48139 | ExpressionAtlas
Project description:NOD mice spontaneously develop lacrimal gland inflammation. NOD mice that lack TLR7 or that lack IFNAR1 are protected from developing lacrimal gland inflammation. RNA sequencing studies were performed to compare gene expression profiles in lacrimal glands from wild-type (WT) vs Tlr7 knockout or Ifnar1 knockout nonobese diabetic (NOD) mice to determine disease-relevant gene and pathway profiles upregulated in WT lacrimal glands in either a TLR7- or IFNAR1-dependent manner.
2021-01-04 | GSE161184 | GEO
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: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:Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease characterized by reduced activity of the exocrine glands (principally the salivary and lacrimal glands) due to chronic lymphocytic infiltration. pSS has been closely associated with an enhanced risk of mucosa-associated lymphoid tissue (MALT) lymphoma. However, the dynamic epigenetic changes in gland cells accompanied with this pathogenesis are not fully understood. In present study, the labial gland (LG) and parotid gland (PG) tissues from two pSS patients with lymphoma were harvested including LG with negative antinuclear antibodies (ANA) and LG with positive ANA at the first diagnosis of pSS, as well as PG with and without lymphoma tissues at the second diagnosis of MALT. RNA-seq of these tissues were studied. This data is benefit to advanced understanding the dynamic development of MALT from pSS, emphasizing the importance of epigenetic alterations in regulating transcription during the pathologic process.
2021-04-17 | E-MTAB-10339 | biostudies-arrayexpress