Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA106769 | ENA |
REPOSITORIES: ENA
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Project description:C57BLKS/J mice are susceptible to diabetes, because of islet dysfunction, whereas C57BL6/J mice are not. Differences in gene expression between the two strains may account for this sensitivity. Furthermore these differences may only be evident in the hyperstimulated (diabetic or hyperglycemic) state. To this end profiling islets from these two strains cultured in both low and high glucose may reveal the underlying mechanism. Keywords: Mouse strain comparison under different culture conditions In the study presented here, pancreatic islets from 20 mice grown in low and high glucose conditions were assayed for differences in gene expression. (five C57BLKS/J low glucose, four C57BLKS/J high glucose, six C57BL6/J low glucose, five C57BL6/J high glucose). Technical replicates are achieved by labeling each sample with both Cy3 and Cy5, and combining the values for each hybridization.
2008-12-30 | E-GEOD-11257 | biostudies-arrayexpress
Project description:The primary driver of Type I diabetes are the autoimmune T cells that destroy insulin-producing beta-cells within the islets of Langerhans in the pancreas. Pancreatic macrophages have also been variably linked to disease onset and progression. As macrophage-mediated removal of dying cells via ‘efferocytosis’ regulate tissue homeostasis and immune responses, we addressed whether efferocytosis by intra-islet macrophages influences the immune environment of pancreatic islets. Here, using a series of complementary omics-based and functional approaches, we identify a subset of anti-inflammatory intra-islet ‘efferocytic macrophages’ (e-Mac) within the pancreas of mice and humans. When limited beta-cell apoptosis is induced in vivo in wild type C57BL/6 mice and diabetic-prone NOD mice, islet macrophages adopt this e-Mac phenotype without an apparent increase in total intra-islet macrophage numbers. Strikingly, such induction of limited beta-cell apoptosis and increase in e-Mac numbers in NOD mice led to long-term suppression of autoimmune diabetes. These data advance a concept that efferocytosis-associated reprogramming of the islet macrophages and its subsequent influence on the adaptive immune response could be beneficial in modulating diabetic autoimmunity.
2025-08-09 | GSE304616 | GEO
Project description:The primary driver of Type I diabetes are the autoimmune T cells that destroy insulin-producing beta-cells within the islets of Langerhans in the pancreas. Pancreatic macrophages have also been variably linked to disease onset and progression. As macrophage-mediated removal of dying cells via ‘efferocytosis’ regulate tissue homeostasis and immune responses, we addressed whether efferocytosis by intra-islet macrophages influences the immune environment of pancreatic islets. Here, using a series of complementary omics-based and functional approaches, we identify a subset of anti-inflammatory intra-islet ‘efferocytic macrophages’ (e-Mac) within the pancreas of mice and humans. When limited beta-cell apoptosis is induced in vivo in wild type C57BL/6 mice and diabetic-prone NOD mice, islet macrophages adopt this e-Mac phenotype without an apparent increase in total intra-islet macrophage numbers. Strikingly, such induction of limited beta-cell apoptosis and increase in e-Mac numbers in NOD mice led to long-term suppression of autoimmune diabetes. These data advance a concept that efferocytosis-associated reprogramming of the islet macrophages and its subsequent influence on the adaptive immune response could be beneficial in modulating diabetic autoimmunity.
2025-08-09 | GSE304628 | GEO
Project description:The primary driver of Type I diabetes are the autoimmune T cells that destroy insulin-producing beta-cells within the islets of Langerhans in the pancreas. Pancreatic macrophages have also been variably linked to disease onset and progression. As macrophage-mediated removal of dying cells via ‘efferocytosis’ regulate tissue homeostasis and immune responses, we addressed whether efferocytosis by intra-islet macrophages influences the immune environment of pancreatic islets. Here, using a series of complementary omics-based and functional approaches, we identify a subset of anti-inflammatory intra-islet ‘efferocytic macrophages’ (e-Mac) within the pancreas of mice and humans. When limited beta-cell apoptosis is induced in vivo in wild type C57BL/6 mice and diabetic-prone NOD mice, islet macrophages adopt this e-Mac phenotype without an apparent increase in total intra-islet macrophage numbers. Strikingly, such induction of limited beta-cell apoptosis and increase in e-Mac numbers in NOD mice led to long-term suppression of autoimmune diabetes. These data advance a concept that efferocytosis-associated reprogramming of the islet macrophages and its subsequent influence on the adaptive immune response could be beneficial in modulating diabetic autoimmunity.
2025-08-09 | GSE304620 | GEO
Project description:Gene expression profiling of pancreatic stem cell derived islet like clusters vs native islets
| PRJNA258195 | ENA
Project description:Expression of cytokine-sensitive genes in islets from diabetes-prone mice
| PRJNA265865 | ENA
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:C57BLKS/J mice are susceptible to diabetes, because of islet dysfunction, whereas C57BL6/J mice are not. Differences in gene expression between the two strains may account for this sensitivity. Furthermore these differences may only be evident in the hyperstimulated (diabetic or hyperglycemic) state. To this end profiling islets from these two strains cultured in both low and high glucose may reveal the underlying mechanism. Keywords: Mouse strain comparison under different culture conditions
2008-12-31 | GSE11257 | GEO
Project description:The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)
| PRJNA252783 | ENA
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
2014-12-04 | GSE61417 | GEO