<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Robert Hume</submitter><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><organism>Homo sapiens</organism><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16453</full_dataset_link><description>Background: Myocardial infarction (MI) is a leading cause of death worldwide and can eliminate up to a third of the cardiomyocytes (CMs) within the human heart. Although CMs undergo mitosis during early development, most CMs cease cell cycling soon after birth. In contrast, rodent MI models have shown that CMs increase mitosis in response to ischemia, however this has not been shown in humans. Methods: Using a unique pre-mortem post-MI human heart, immunostaining, bulk RNA sequencing, proteomics, metabolomics, single nucleus RNA sequencing and a novel post-MI human biopsy method, we investigated human CM mitosis post-MI. Results: We show that adult human CMs exhibit increased mitosis and cytokinesis in response to ischemia. Conclusions: Future development of therapeutics to enhance this intrinsic mitotic potential could lead to new treatments that reverse heart failure via cardiac regeneration.  This dataset is the bulk RNAseq dataset relating to a unique infarcted heart - left ventricle (6004 LV), right ventricle (6004 RV), right atrium (6004 RA) and healthy donor left ventricle (donor LV).</description><repository>biostudies-arrayexpress</repository><sample_protocol>Nucleic Acid Extraction - Approximately 50mg of tissue/sample was disrupted using a metal bead (Qiagen #69989) in a 2mL tubes with 500uL TRIzol (Ambion #15596018) using the TissueLyser LT (Qiagen) and RNA extraction performed according to TRIzol manufacturer’s instructions. DNA removal was performed using Qiagen RNAse-Free DNase kit (Qiagen #79254) and purified using the RNeasy Mini kit (Qiagen, #74104) according to manufacturer’s instructions. RNA quality was evaluated using a Nanodrop and an RNA Nano Chip (Agilent #5067-1511) on an Agilent Bioanalyzer. Libraries were prepared with Illumina Stranded Total RNA prep Ligation with Ribo Zero Plus kit, according to manufacturer’s instructions. Libraries were sequenced using a paired-end 250bp Illumina NovaSeq 6000 S4 flow cell.</sample_protocol><sample_protocol>Sample Collection - Premortem cardiac samples were collected from the left ventricle (LV) right ventricle (RV) or right atrium (RA) within 15 minutes via snap freezing in liquid nitrogen</sample_protocol><sample_protocol>Library Construction - Approximately 50mg of tissue/sample was disrupted using a metal bead (Qiagen #69989) in a 2mL tubes with 500uL TRIzol (Ambion #15596018) using the TissueLyser LT (Qiagen) and RNA extraction performed according to TRIzol manufacturer’s instructions. DNA removal was performed using Qiagen RNAse-Free DNase kit (Qiagen #79254) and purified using the RNeasy Mini kit (Qiagen, #74104) according to manufacturer’s instructions. RNA quality was evaluated using a Nanodrop and an RNA Nano Chip (Agilent #5067-1511) on an Agilent Bioanalyzer. Libraries were prepared with Illumina Stranded Total RNA prep Ligation with Ribo Zero Plus kit, according to manufacturer’s instructions. Libraries were sequenced using a paired-end 250bp Illumina NovaSeq 6000 S4 flow cell.</sample_protocol><sample_protocol>Sequencing - Approximately 50mg of tissue/sample was disrupted using a metal bead (Qiagen #69989) in a 2mL tubes with 500uL TRIzol (Ambion #15596018) using the TissueLyser LT (Qiagen) and RNA extraction performed according to TRIzol manufacturer’s instructions. DNA removal was performed using Qiagen RNAse-Free DNase kit (Qiagen #79254) and purified using the RNeasy Mini kit (Qiagen, #74104) according to manufacturer’s instructions. RNA quality was evaluated using a Nanodrop and an RNA Nano Chip (Agilent #5067-1511) on an Agilent Bioanalyzer. Libraries were prepared with Illumina Stranded Total RNA prep Ligation with Ribo Zero Plus kit, according to manufacturer’s instructions. Libraries were sequenced using a paired-end 250bp Illumina NovaSeq 6000 S4 flow cell.</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><pubmed_authors>Robert Hume</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNAseq of a unique human heart 5 days post-myocardial infarction versus healthy donor controls</name><description>Background: Myocardial infarction (MI) is a leading cause of death worldwide and can eliminate up to a third of the cardiomyocytes (CMs) within the human heart. Although CMs undergo mitosis during early development, most CMs cease cell cycling soon after birth. In contrast, rodent MI models have shown that CMs increase mitosis in response to ischemia, however this has not been shown in humans. Methods: Using a unique pre-mortem post-MI human heart, immunostaining, bulk RNA sequencing, proteomics, metabolomics, single nucleus RNA sequencing and a novel post-MI human biopsy method, we investigated human CM mitosis post-MI. Results: We show that adult human CMs exhibit increased mitosis and cytokinesis in response to ischemia. Conclusions: Future development of therapeutics to enhance this intrinsic mitotic potential could lead to new treatments that reverse heart failure via cardiac regeneration.  This dataset is the bulk RNAseq dataset relating to a unique infarcted heart - left ventricle (6004 LV), right ventricle (6004 RV), right atrium (6004 RA) and healthy donor left ventricle (donor LV).</description><dates><release>2025-12-31T00:00:00Z</release><modification>2025-12-31T02:03:18.153Z</modification><creation>2025-12-19T13:39:41.246Z</creation></dates><accession>E-MTAB-16453</accession><cross_references><ENA>ERP186839</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>