Project description:This SuperSeries is composed of the following subset Series: GSE41706: Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates GSE41807: Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice GSE41808: Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice. GSE41809: Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates Refer to individual Series
Project description:We performed time-series single-cell RNA-seq analysis of blood CD11b+ cells and of the inflammatory infiltrate in the heart of C57BL/6J male mice in a model of permanent myocardial infarction.
Project description:The aims of the experiment were to profile the cardiac interstitial (non-myocyte) cell types in the adult mouse from injured and uninjured hearts and how they respond to modulation of platelet-derived growth factor receptor alpha (PDGFRa) signaling. Adult, male, C57BL/BJ mice were subject to either a myocardial infarction or sham injury, and given either PDGF-AB or PBS treatment via mini-pump, with single-cell RNA-seq profiles obtained from interstitial cells isolated from cardiac ventricles 3 or 7 days following surgery.
Project description:In order to study the changes of liver protein level in mice with acute cardiac rejection, we established a mouse model of ectopic heart transplantation. According to the matching relationship between recipient and donor, they were divided into the following two groups: allograft group (ALLO), BALB/ C hearts were transplanted into C57BL/6J recipients with complete mismatch of major histocompatibility complex; In the syngeneic transplantation group (ISO), C57BL/6J hearts were transplanted into MHC-matched C57BL/6J recipients. On day 6 after mouse heart transplantation, livers were obtained from recipient mice in the allograft group (n = 3) and from recipient mice in the syngeneic (ISO) group (n = 3). A series of techniques such as protein extraction, enzyme digestion, TMT labeling, HPLC classification, liquid chromatography-mass spectrometry tandem analysis, database search and bioinformation analysis were used to study the quantitative proteome of samples.
Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.