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Transcriptome-wide mRNA alterations in Streptozotocin induced Type I diabetic mouse heart

ABSTRACT: We sequenced mRNA from Left Ventricles of Streptozotocin induced Type I diabetic mouse hearts or mock treated controls at 4 weeks post-treatment in order to assess alternative splicing changes.

ORGANISM(S): Mus musculus

PROVIDER: GSE80664 | GEO | 2016/05/26

SECONDARY ACCESSION(S): PRJNA321413

REPOSITORIES: GEO

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diabetic nephropathy streptozotocin db db

Project description:diabetes, mouse models, diabetic nephropathy, streptozotocin db/db Keywords: other

2004-01-20 | GSE710 | GEO

Transcription profiling of rat ventricle samples from streptozotocin (STZ)-diabetic animals to investigate mitochondrial long-chain free fatty acid export

Project description:Cardiomyopathy in type 1 diabetic patients is characterized by early onset diastolic and late onset systolic dysfunction. The mechanism underlying development of diastolic and systolic dysfunction in diabetes remains unknown. We used microarrays to detail the ventricle gene expression changes that underly development of diabetic cardiomyopathy. We identified distinct classes of up-regulated genes during this process. Experiment Overall Design: 150g male Wistar rats (Harlan) we injected with 65 mg/kg streptozotocin to induce Type 1 diabetes. Four replicates of Control and Diabetic rat ventricles were removed and frozen at Three time points for total RNA isolation and hybridization on the Affymetrix RG-U34A microarray. The 3 day samples show a baseline for initial diabetic changes in the ventricle. The 28 day samples show changes associated with diastolic dysfunction in diabetes. The 42 day samples show changes associated with both diastolic and systolic dysfunction in type 1 diabetic rat ventricles.

2007-11-29 | E-GEOD-4745 | biostudies-arrayexpress

Enarodustat, hypoxia-inducible factor stabilizer, counteracts the diabetic renal energy metabolism alterations in streptozotocin-induced diabetic rats

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2020-05-14 | GSE131221 | GEO

Transcription profiling of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

Project description:A study of diabetic neuropathy in dorsal root ganglia from streptozotocin-diabetic male wistar rats over the first 8 weeks of diabetes

2006-12-10 | E-MEXP-515 | biostudies-arrayexpress

Transcription profiling of rat left ventricle treated with streptozotocin vs. controls

Project description:8 week old rats injected with streptozotocin or buffer alone at age of 8 weeks, heart obtained at 12 weeks (thus animals were diabetic for 4 weeks). Left vent of heart. Experiment Overall Design: Three control rats (normal heart #1, 2, 3) Experiment Overall Design: Three diabetic rats (diabetic heart #1, 2, 3)

2008-06-15 | E-GEOD-6880 | biostudies-arrayexpress

Single cell RNA sequencing (scRNA-Seq) deciphering pathological alterations in streptozotocin-induced diabetic retinas

Project description:Diabetic retinopathy (DR) is an irreversible and progressive diabetic complication leading to visual impairment, even blindness. Due to the delicate and complicated structure of the retina, the pathology of DR has not been completely elucidated yet. We constructed a transcriptome atlas of >14,000 single cells from healthy and streptozotocin (STZ)-induced diabetic murine retinas to decipher pathological alterations of DR. We found four stress-inducible genes Cirbp, Rmb3, Mt1 and Mt2 commonly induced in most types of retinal cells. Bipolar cells were little affected both in number and gene expression. There existed two subtypes of Müller cells, the Fos-expressing subtype and the no-marker subtype, and the latter lost more in DR. A large number of genes were deregulated in diabetic vascular endothelial cells (ECs), and the differential expression genes were paired to the pathways functioning in metabolism, shear stress and vascular permeability. These pathways were mapped by more differential expression genes in a subpopulation of ECs specifically presented in diabetic retinas (diabetic retinal ECs, DRECs). Moreover, several inflammation pathways were activated in DRECs, and the most significant one is the IL-17 signaling pathway. According to the EC markers, DRECs were mainly capillary ECs, confirmed by immunofluorescent staining of S100a9, a target gene of the IL-17 signaling pathway. This study deciphered pathological alterations of DR, and provided clues for new potential targets for DR therapy.

2021-08-24 | GSE178121 | GEO

Atorvastatin Reduces Î²-Adrenergic Dysfunction in Rats with Diabetic Cardiomyopathy

Project description:Background: In the diabetic heart the Î²-adrenergic response is altered partly by down-regulation of the Î²1-adrenoceptor, reducing its positive inotropic effect and up-regulation of the Î²3-adrenoceptor, increasing its negative inotropic effect. Statins have clinical benefits on morbidity and mortality in diabetic patients which are attributed to âpleiotropicâ effects. The objective of our study was to investigate the role of statin treatment on Î²-adrenergic dysfunction in diabetic rat cardiomyocytes. Methods: Î²-adrenergic responses were investigated in vivo (echocardiography) and ex vivo (left ventricular papillary muscles) in healthy and streptozotocin-induced diabetic rats, who were pre-treated or not by oral atorvastatin over 15 days (50 mg.kg-1.day-1). Micro-array analysis and immunoblotting were performed in left ventricular homogenates. Data are presented as mean percentage of baseline Â± SD. Results: Atorvastatin restored the impaired positive inotropic effect of Î²-adrenergic stimulation in diabetic hearts compared with healthy hearts both in vivo and ex vivo but did not suppress the diastolic dysfunction of diabetes. Atorvastatin changed the RNA expression of 9 genes in the Î²-adrenergic pathway and corrected the protein expression of Î²1-adrenoceptor and Î²1/Î²3-adrenoceptor ratio, and multidrug resistance protein 4 (MRP4). Nitric oxide synthase (NOS) inhibition abolished the beneficial effects of atorvastatin on the Î²-adrenoceptor response. Conclusions: Atorvastatin restored the positive inotropic effect of the Î²-adrenoceptor stimulation in diabetic cardiomyopathy. This effect is mediated by multiple modifications in expression of proteins in the Î²-adrenergic signaling pathway, particularly through the NOS pathway.

2017-06-27 | E-MTAB-5594 | biostudies-arrayexpress

Differential gene expression in liver tissues of streptozotocin-induced diabetic rats in response to resveratrol treatment

Project description:This study was conducted to elucidate the genome-wide gene expression profile in streptozotocin induced diabetic liver tissues in response to resveratrol treatment.

2015-03-11 | E-MTAB-3293 | biostudies-arrayexpress

Heart in Diabetes

2008-01-26 | GSE6880 | GEO

Streptozotocin-induced Type 1 and 2 Diabetes Mellitus Mouse Models Show Different Functional, Cellular and Molecular Patterns of Diabetic Cardiomyopathy

Project description:The main cause of morbidity and mortality in diabetes mellitus (DM) are cardiovascular complications. Diabetic cardiomyopathy (DCM) remains incompletely understood. Animal models have been crucial in exploring DCM pathophysiology while identifying potential therapeutic targets. Streptozotocin (STZ) has been widely used to produce experimental models of both type 1 and type 2 DM (T1DM and T2DM). Here we compared these two models for their effects on cardiac structure, function, and transcriptome. Different doses of STZ and different diet chows were used to generate T1DM and T2DM in C57BL/6J mice. Normal euglycemic and non-obese sex and age-matched mice served as controls (CTRL). Immunohistochemistry, RT-PCR, and RNA-Seq were employed to compare hearts from the three animal groups. STZ-induced T1DM and T2DM differently affect left ventricular function and myocardial performance. T1DM displays an exaggerated apoptotic cardiomyocyte (CM) death and reactive hypertrophy and fibrosis along with increased cardiac oxidative stress, CM DNA damage and senescence when compared to T2DM mice. T1DM and T2DM differently affect whole cardiac transcriptome. In conclusion, STZ-induced T1DM and T2DM mouse models show significant differences in cardiac remodeling, function and whole transcriptome. These differences could be of key relevance when choosing an animal model to study specific features of DCM.

2023-02-20 | E-MTAB-12558 | biostudies-arrayexpress

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