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DNA array analysis in OLETF, a type 2 diabetic rats, and LETO, a non-diabetic control rats

ABSTRACT: AMP deaminase (AMPD) plays a crucial role in adenine nucleotide metabolism, and its upregulated activity contributes to diastolic dysfunction of the heart caused by type 2 diabetes mellitus (T2DM) via reduction of the adenine nucleotide pool. Here we examined the mechanism of AMPD upregulation by T2DM. The protein level of 90-kDa full-length AMPD3 was increased in whole myocardial lysates and in the sarcoplasmic reticulum (SR) fraction by 55% and 123%, respectively, in OLETF, a rat model of T2DM, compared to those in LETO, a non-diabetic control, though AMPD mRNA level was unchanged in OLETF. MicroRNA array analysis revealed downregulation (>50%) of 57 microRNAs in OLETF compared to those in LETO, among which miR-301b was predicted to interact with the 3’UTR of AMPD3 mRNA. The 90-kDa AMPD3 level was significantly increased by miR-301b inhibitor, but decreased by a miR-301b mimetic in H9c2 cells. A luciferase reporter assay indicated binding of miR-301b to the 3’UTR of AMPD3 mRNA. The results indicate that translational regulation by miR-301b mediates AMPD3 upregulation in the diabetic heart. Since ATP generated by SR-associated glycolytic enzymes contributes to Ca2+ uptake by SERCA2a, upregulated AMPD3 in the vicinity of the SR may be a therapeutic target for diabetic cardiomyopathy.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE99203 | GEO | 2017/05/24

SECONDARY ACCESSION(S): PRJNA387556

REPOSITORIES: GEO

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Micro RNA array analysis in OLETF, a type 2 diabetic rats, and LETO, a non-diabetic control rats

Project description:AMP deaminase (AMPD) plays a crucial role in adenine nucleotide metabolism, and its upregulated activity contributes to diastolic dysfunction of the heart caused by type 2 diabetes mellitus (T2DM) via reduction of the adenine nucleotide pool. Here we examined the mechanism of AMPD upregulation by T2DM. The protein level of 90-kDa full-length AMPD3 was increased in whole myocardial lysates and in the sarcoplasmic reticulum (SR) fraction by 55% and 123%, respectively, in OLETF, a rat model of T2DM, compared to those in LETO, a non-diabetic control, though AMPD mRNA level was unchanged in OLETF. MicroRNA array analysis revealed downregulation (>50%) of 57 microRNAs in OLETF compared to those in LETO, among which miR-301b was predicted to interact with the 3’UTR of AMPD3 mRNA. The 90-kDa AMPD3 level was significantly increased by miR-301b inhibitor, but decreased by a miR-301b mimetic in H9c2 cells. A luciferase reporter assay indicated binding of miR-301b to the 3’UTR of AMPD3 mRNA. The results indicate that translational regulation by miR-301b mediates AMPD3 upregulation in the diabetic heart. Since ATP generated by SR-associated glycolytic enzymes contributes to Ca2+ uptake by SERCA2a, upregulated AMPD3 in the vicinity of the SR may be a therapeutic target for diabetic cardiomyopathy.

2017-05-31 | GSE99410 | GEO

miRNA expression profiles in the serum of diabetic cats

Project description:BACKGROUND: MicroRNAs negatively regulate gene expression and play a pivotal role in the pathogenesis of human type 2 diabetes mellitus (T2DM). As the domestic cat presents a spontaneous animal model for human T2DM, the purpose of this study was to investigate whether microRNAs are detectable in feline serum and whether microRNA expression profiles differ between healthy and diabetic cats. METHODS: Total RNA was extracted from 400 M-BM-5l serum of healthy lean (HL) and newly diagnosed diabetic (D) cats. MicroRNA microarrays representing 1079 distinct mouse miRNA targets were used to measure miRNA expression in samples from eight HL and eight D cats. RESULTS: By microarray, 227 distinct microRNAs were identified. Nineteen miRNAs were differentially expressed in diabetic cats, but only two reached statistical significance after correction for multiple comparisons. In qRT-PCR, miR-122* was found to be upregulated in diabetic cats more than 40-fold compared to HL cats, while miR-193b was upregulated about 10-fold. MiR-483* showed a 6- fold increase in diabetic cats compared to HL cats. CONCLUSIONS: Small volumes of serum samples yield sufficient material to detect altered microRNA expression profiles in diabetic cats. The domestic cat may be considered a useful animal model for studying miRNAs involved in human T2DM. Blood was drawn from two groups of cats: 8 healthy cats and 8 cats suffering from diabetes. After clotting, samples were centrifuged and total mRNA was extracted from serum. These 16 serum samples were analyzed and the groups were compared. Due to technical problems during hybridization (leaking chamber), sample 1_4_B (Serum_diabetic_8) was not included into analysis.

2013-04-11 | E-GEOD-37177 | biostudies-arrayexpress

CircARHGAP12 triggers MSC autophagy to facilitate its effect on repairing diabetic wounds by sponging miR-301b-3p/ATG16L1 and miR-301b-3p/ULK2

Project description:Circular RNAs (circRNAs) have been found to play critical roles in the development and progression of human diseases. However, the role of circRNAs in regulating MSCs (mesenchymal stromal cells) to repair diabetic wounds remains unclear. Here, we showed that MSCs subjected to high glucose stress showed an obvious decrease in circARHGAP12, while circARHGAP12-mediated autophagy inhibited high glucose-induced apoptosis of MSCs. Mechanistically, circARHGAP12 could directly interact with miR-301b-3p, and subsequently act as a miRNA sponge to regulate the expression of the miR-301b-3p target genes ATG16L1 and ULK2 and the downstream signaling pathway. Furthermore, circARHGAP12 led to a decrease in apoptosis of MSCs in wounds and promoted wound healing. Taken together, these data indicated that circARHGAP12/ miR-301b-3p/ATG16L1 and ULK2 regulatory networks may be a potential therapeutic target for MSCs in repairing diabetic wounds.

2021-03-15 | GSE168890 | GEO

miRNA expression profiles in the serum of diabetic cats

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2013-04-11 | GSE37177 | GEO

Transcriptome analysis of diabetic and non diabetic patients affected by post-ischemic heart failure

Project description:Increased morbidity and mortality associated with post-ischemic heart failure (HF) in diabetic patients underscore the need for a better understanding of the underlying molecular events. Indeed, effective HF therapy in diabetic patients requires a complex strategy encompassing the development of improved diagnostic and prognostic markers and innovative pharmacological approaches. Whole mRNAs expression was measured in the heart of patients with heart failure (HF) with or without concomitant Type 2 diabetes mellitus (T2DM) and compared it to control non-failing hearts. We identified distinct genes modulated in HF patients compared to controls, as well as to T2DM HF patients compared to not diabetic HF patients. Our study included left ventricle (LV) cardiac biopsies taken from the vital, non-infarcted zone (remote zone) derived from patients affected by dilated hypokinetic post-ischemic cardiomyopathy, undergoing surgical ventricular restoration procedure. Inclusion criteria for diabetic were: GLICEMIA: >=126 mg/dl, previous T2DM diagnosis or anti-diabetic therapy, while for non diabetic: GLICEMIA: <100 mg/dl and HbA1c: n.v. 4.8-6.0%. Moreover, HF patients were matched for End Systolic Volume (ESV), Ejection fraction (LVEF), Age, Sex, Ethnic distribution, Smoke habits, Hypertension, Glomerular filtration rate (GFR), Body Mass Index (BMI). Genes expression was assessed by Affymetrix GeneChips Human Gene 1.0 ST array, using total RNA extracted from 7 T2DM HF patients, 12 non-T2DM HF patients and 5 controls.

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Transcriptome analysis of diabetic and non diabetic patients affected by post-ischemic heart failure

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A potential study model seeking for proteins related to dental implant failure of type 2 diabetic patients estabilished by proteomics.

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2021-11-02 | PXD016489 | Pride

CircARHGAP12 triggers MSC autophagy to facilitate its effect on repairing diabetic wounds by sponging miR-301b-3p/ATG16L1 and miR-301b-3p/ULK2

Project description:CircARHGAP12 triggers MSC autophagy to facilitate its effect on repairing diabetic wounds by sponging miR-301b-3p/ATG16L1 and miR-301b-3p/ULK2

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Project description:Type 2 diabetes mellitus (T2DM) is a complex disease characterized by the inability of the insulin-producing β-cells in the endocrine pancreas to overcome insulin resistance in peripheral tissues. To determine if microRNAs are involved in the pathogenesis of human T2DM, we sequenced the small RNAs of human islets from diabetic and non-diabetic organ donors. We identified a cluster of miRNAs in an imprinted locus on human chromosome 14q32 that is highly and specifically expressed in human β-cells and dramatically down-regulated in islets from T2DM organ donors. The down-regulation of this locus strongly correlates with hyper-methylation of its promoter. Using HITS-CLIP for the essential RISC-component Argonaute, we identified disease-relevant targets of the chromosome 14q32 microRNAs, such as IAPP and TP53INP1 that cause increased β-cell apoptosis upon over-expression in human islets. Our results support a role for microRNAs and their epigenetic control by DNA methylation in the pathogenesis of T2DM. Identification of miRNA-target interaction in human islets using HITS-CLIP, one mRNA library and one miRNA library

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