<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Dunja Aksentijevic</submitter><organism>Mus musculus</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-13849</full_dataset_link><description>Chronic inflammation is a hallmark of obesity type II diabetes (T2D) accompanied by increased circulating inflammatory T-cells. Diabetic cardiomyopathy (dbCM) is characterised by systemic inflammation, disrupted metabolism and impaired cardiac function. However, whether T-cell mediated cardiac autoimmunity is present in dbCM and causally linked to cardiac metabolic remodelling remains unknown. We used db/db transgenic mouse model of dbCM and an integrated in vivo and ex vivo experimental approach to examine the impact of T-cell mediated inflammation on cardiac function and metabolic disturbances in T2D. Furthermore, we used  glucokinase activator AZD1656 drug intervention for six weeks in db/db mice to examine whether we can improve metabolic remodeling and cardiac inflammation in dbCM. This drug has been previously shown to target metabolism of T cells and with anti-inflammatory effect.  In this data set, we used RNA extracted from the snap-frozen hearts (control, db/db and AZD1656-treated db/db hearts, n=5/group) analysed by massive analysis of cDNA End (MACE-Seq, 1x75 bps Illumina; MACE: 5 Million reads / library).</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sample Collection - Mice were terminally anaesthetized, hearts rapidly excised into ice cold PBS and freeze-clamped using wollenberger tongs.</sample_protocol><sample_protocol>Library Construction - Rapid MACE-seq was used to prepare 3’ RNA sequencing libraries. Samples of 100 ng of DNA-depleted RNA were used for library preparation, using the Rapid MACE-Seq kit (GenXPro GmbH, Germany). Fragmented RNA underwent reverse transcription using barcoded oligo(dT) primers containing TrueQuant unique molecular identifiers, followed by template switching. PCR amplified libraries were purified by solid phase reversible immobilization beads and subsequent sequencing was performed using the Illumina platform NextSeq 500. Unprocessed sequencing reads were adapter-trimmed and quality-trimmed using Cutadapt (version 3.4). Deduplication based on UMIs (Unique Molecular Identifier) was performed using in-house tools. FastQC (0.11.9) was used to assess the quality of sequencing reads. MultiQC (version 1.16) was used to create a single report visualising output from multiple tools across many samples, enabling global trends and biases to be quickly identified.</sample_protocol><sample_protocol>Nucleic Acid Extraction - RNA extracted from the snap-frozen hearts was analysed by massive analysis of cDNA End (MACE-Seq, 1x75 bps Illumina; MACE: 5 Million reads / library). MACE-Seq was annotated, reads quantified and p values for differential expression generated by GenXPro (Frankfurt, Germany).</sample_protocol><sample_protocol>Sequencing - RNA extracted from the snap-frozen hearts was analysed by massive analysis of cDNA End (MACE-Seq, 1x75 bps Illumina; MACE: 5 Million reads / library).</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina Genome Analyzer</instrument_platform><instrument_platform>Wollenberger tongs</instrument_platform><study_type>RNA-seq of coding RNA</study_type><species>Mus musculus</species><pubmed_title>Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy</pubmed_title><pubmed_authors>Dunja Aksentijevic</pubmed_authors></additional><is_claimable>false</is_claimable><name>Myocardial gene expression of type 2 diabetic mice with and without treatment with glucokinase activator</name><description>Chronic inflammation is a hallmark of obesity type II diabetes (T2D) accompanied by increased circulating inflammatory T-cells. Diabetic cardiomyopathy (dbCM) is characterised by systemic inflammation, disrupted metabolism and impaired cardiac function. However, whether T-cell mediated cardiac autoimmunity is present in dbCM and causally linked to cardiac metabolic remodelling remains unknown. We used db/db transgenic mouse model of dbCM and an integrated in vivo and ex vivo experimental approach to examine the impact of T-cell mediated inflammation on cardiac function and metabolic disturbances in T2D. Furthermore, we used  glucokinase activator AZD1656 drug intervention for six weeks in db/db mice to examine whether we can improve metabolic remodeling and cardiac inflammation in dbCM. This drug has been previously shown to target metabolism of T cells and with anti-inflammatory effect.  In this data set, we used RNA extracted from the snap-frozen hearts (control, db/db and AZD1656-treated db/db hearts, n=5/group) analysed by massive analysis of cDNA End (MACE-Seq, 1x75 bps Illumina; MACE: 5 Million reads / library).</description><dates><release>2025-12-04T00:00:00Z</release><modification>2025-12-04T13:08:26.44Z</modification><creation>2024-02-23T10:07:02.87Z</creation></dates><accession>E-MTAB-13849</accession><cross_references><ENA>ERP157691</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>