Project description:We report an integrative analysis of miRNA-seq and mRNA-seq to identify miRNAs, genes, and miRNA-mRNA interactions for human atrial aging (AA). We found that seven miRNAs (4 upregulation and 3 downregulation) and 42 genes (23 upregulation and 19 downregulation) show differential expression between older samples and younger samples in human right atrial tissues. Pearson correlation analysis identified 114 pairs of putative miRNA-mRNA interactions for AA. Pathway enrichment analysis identified three important pathways including rhythmic process, senescence and autophagy in cancer, and positive regulation of cytokine biosynthetic process. Our study revealed novel miRNA-mRNA interaction networks and signaling pathways for AA, providing novel insights into the development of human AA. This dataset includes data generation and processing steps for the mRNA-seq data generated from twelve SR samples.
Project description:We report an integrative analysis of miRNA-seq and mRNA-seq to identify miRNAs, genes, and miRNA-mRNA interactions for human atrial aging (AA). We found that seven miRNAs (4 upregulation and 3 downregulation) and 42 genes (23 upregulation and 19 downregulation) show differential expression between older samples and younger samples in human right atrial tissues. Pearson correlation analysis identified 114 pairs of putative miRNA-mRNA interactions for AA. Pathway enrichment analysis identified three important pathways including rhythmic process, senescence and autophagy in cancer, and positive regulation of cytokine biosynthetic process. Our study revealed novel miRNA-mRNA interaction networks and signaling pathways for AA, providing novel insights into the development of human AA. This dataset includes data generation and processing steps for the miRNA-seq data generated from twelve SR samples.
Project description:Skeletal muscle degenerates progressively, loses mass (sarcopenia) along in years, and leads to reduced physical ability, often causing secondary diseases such as diabetes and obesity. It is known that regulation of gene expression by microRNAs is a key event in muscle development and disease. To understand genome-wide changes in microRNAs and mRNAs during muscle aging, we sequenced microRNAs as well as mRNAs from mouse gastrocnemius muscles at two different ages (6 versus 24-month-old). Thirty-four microRNAs (15 up-regulated and 19 down-regulated) were differentially expressed with age among which were microRNAs such as miR-206 or -434 which were differentially expressed in aged muscle in previous studies. Interestingly, seven microRNAs in a microRNA cluster at imprinted Dlk1-Dio3 locus on chromosome 12 were coordinately down-regulated. In addition, sixteen novel microRNAs were identified. Integrative analysis of microRNA and mRNA expression revealed that microRNAs contribute to muscle aging possibly through the positive regulation of transcription, metabolic process, and kinase activity. Many of the age-related microRNAs were implicated in human muscular diseases. We suggest that genome-wide microRNA profiling helps to expand our knowledge of microRNA function in the muscle aging process. mRNA profiles of gastrocnemius muscle tissues (n=10) were generated by deep sequencing using Illumina Hiseq-2000
Project description:Skeletal muscle degenerates progressively, loses mass (sarcopenia) along in years, and leads to reduced physical ability, often causing secondary diseases such as diabetes and obesity. It is known that regulation of gene expression by microRNAs is a key event in muscle development and disease. To understand genome-wide changes in microRNAs and mRNAs during muscle aging, we sequenced microRNAs as well as mRNAs from mouse gastrocnemius muscles at two different ages (6 versus 24-month-old). Thirty-four microRNAs (15 up-regulated and 19 down-regulated) were differentially expressed with age among which were microRNAs such as miR-206 or -434 which were differentially expressed in aged muscle in previous studies. Interestingly, seven microRNAs in a microRNA cluster at imprinted Dlk1-Dio3 locus on chromosome 12 were coordinately down-regulated. In addition, sixteen novel microRNAs were identified. Integrative analysis of microRNA and mRNA expression revealed that microRNAs contribute to muscle aging possibly through the positive regulation of transcription, metabolic process, and kinase activity. Many of the age-related microRNAs were implicated in human muscular diseases. We suggest that genome-wide microRNA profiling helps to expand our knowledge of microRNA function in the muscle aging process. miRNA profiles of gastrocnemius muscle tissues (n=10) were generated by deep sequencing using Illumina Hiseq-2000
Project description:Atrial fibrillation (AF) is the most common irregular heart rhythm which influence approximately 1–2% of the general population. As a potential factor for ischemic stroke, AF could also cause heart failure. The mechanisms behind AF pathogenesis are complex and remains elusive. As a new category of non-coding RNAs (ncRNAs), circular RNAs (circRNAs) have been known as the key of developmental processes, regulation of cell function, pathogenesis of heart diseases and pathological responses which could provide novel sight into the pathogenesis of AF. circRNAs function as modulators of microRNAs in cardiac disease. To investigate the regulatory mechanism of circRNA in atrial fibrillation, especially the complex interactions among circRNA, microRNA and mRNA, we collected the heart tissues from three AF patients and three healthy controls and profiled their circRNA expressions with circRNA Microarray. The differentially expressed circRNAs were identified and the biological functions of their interaction microRNAs and mRNAs were analyzed. Our results provided novel insights of the circRNA roles in atrial fibrillation and proposed highly possible interaction mechanisms among circRNAs, microRNAs and mRNAs.
Project description:The transcription factor FOG2 (ZFPM2) is upregulated in human heart failure and increased FOG2 expression causes heart failure in mice. We found that FOG2 directly intersects a gene regulatory network driven by the atrial-enriched TF TBX5 and required for atrial cardiomyocyte rhythm control gene expression