Genomic profiling of type-1 adult diabetic and aged normoglycemic mice liver
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE50613 | GEO | 2013/09/06
SECONDARY ACCESSION(S): PRJNA218093
REPOSITORIES: GEO
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Project description:Here we characterized and compared differential gene expression from diabetic and normoglycemic NOD mice and from aged and young-adults Balb/c mice. Total RNA from NOD diabetic (3 weeks with glicemia over 500mg/dl) and normoglycemic NOD mice from the same age was used. To compare the effects of aging in genomic expression, total RNA from young-adult Balb/c (9 weeks old) and middle-aged Balb/c (47 weeks old) were used.
2013-09-06 | E-GEOD-50613 | biostudies-arrayexpress
Project description:The goal of this study is to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. We found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 (Prmt2-/-) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells by RNA seq. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression.
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Project description:Hybrid insulin peptides (HIPs) result from the linkage of an insulin C-peptide fragment and another peptide via a traditional peptide bond to generate a sequence that is not encoded in the genome. Here, we sought to identify HIPs naturally present in the pancreatic islets of non-obese diabetic (NOD) mice, BALB/c mice, and non-diabetic human donors by mass spectrometry.
2019-01-07 | PXD011606 | Pride
Project description:This a model from the article:
Modelling the onset of Type 1 diabetes: can impaired macrophage phagocytosis make the difference between health and disease?
Maree AF, Kublik R, Finegood DT, Edelstein-Keshet L.Philos Transact A Math Phys Eng Sci.2006 May 15;364(1842):1267-82.
16608707,
Abstract:
A wave of apoptosis (programmed cell death) occurs normally in pancreatic beta-cells of newborn mice. We previously showed that macrophages from non-obese diabetic (NOD) mice become activated more slowly and engulf apoptotic cells at a lower rate than macrophages from control (Balb/c) mice. It has been hypothesized that this low clearance could result in secondary necrosis, escalating inflammation and self-antigen presentation that later triggers autoimmune, Type 1 diabetes (T1D). We here investigate whether this hypothesis could offer a reasonable and parsimonious explanation for onset of T1D in NOD mice. We quantify variants of the Copenhagen model (Freiesleben De Blasio et al. 1999 Diabetes 48, 1677), based on parameters from NOD and Balb/c experimental data. We show that the original Copenhagen model fails to explain observed phenomena within a reasonable range of parameter values, predicting an unrealistic all-or-none disease occurrence for both strains. However, if we take into account that, in general, activated macrophages produce harmful cytokines only when engulfing necrotic (but not apoptotic) cells, then the revised model becomes qualitatively and quantitatively reasonable. Further, we show that known differences between NOD and Balb/c mouse macrophage kinetics are large enough to account for the fact that an apoptotic wave can trigger escalating inflammatory response in NOD, but not Balb/c mice. In Balb/c mice, macrophages clear the apoptotic wave so efficiently, that chronic inflammation is prevented.
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
For more information see the terms of use.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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