Project description:Data set contains 12 samples, 2 genetypes (floxed-HDAC2/ERT2cre) and (WT/ERT2cre), and 2 treatment conditions (no ischemia, 4 hours after 28 min warm ischemia), with three samples each.
Project description:Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3α expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3α in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3α promotes renal fibrosis, we transfected TKPTS cells with Hnf3a overexpression plasmids or control plasmids, and then performed transcriptome sequencing.
Project description:Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3α (also known as FOXA1) expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3α in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3α promotes renal fibrosis, we analyse the genome-wide target sites of HNF3α using CUT&Tag sequencing.
Project description:Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI. we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocyte/macrophage populations by differential expression of Ly6C in CD11b+ cells and to define the function of these cells in the pathophysiology of disease on the basis of microarray gene signatures and reduction strategies
Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model 15 female Yorkshire pigs were divided into three groups: 1: no IPC and 90 minutes warm ischemia; 2: remote IPC with an early window followed by 90 min warm ischemia; 3: remote IPC with a late window followed by warm ischemia 24 hrs later. Kidney tissues were obtained after 72 hours.
Project description:Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI. we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocyte/macrophage populations by differential expression of Ly6C in CD11b+Â cells and to define the function of these cells in the pathophysiology of disease on the basis of microarray gene signatures and reduction strategies Macrophage populations were sorted by Flow Cytometry into low and intermediate populations by Itgam(Cd11b) and Ly6c markers. The cells obtained in 5 weeks sham, 5 weeks IR, 9 day sham, and 9 day IR with 6 samples per group (3 int and 3 low). Cells were sorted in 350ul of RLT lysing buffer and kept at -80c until RNA extraction.Sample amplification, fragmentation, hybridization,washing and scanning were performed according to validated Affymetrix protocol in a CLIA certified lab.
Project description:To investigate the mechanism by which ischemic preconditioning (IPC) produces tissue tolerance to renal ischemia reperfusion injury in a pig model
Project description:Analysis of epigenetic changes of pericytes after ischemia-reperfusion renal injury. The hypothesis tested in the present study was that epigenetic change develope in pericytes after acute kidney injury. This phenotype change would cause pericyte to be more proliferative and profibrotic. Results provide important information of the epigenetic change of pericytes, such as specific mechano-responsive genes, up-regulated specific proliferative and profibrotic functions.
Project description:Time course experiments involving bilateral renal ischemia reperfusion injury (IRI) in C57BL/6J mice (0 hr control, 20 min bilateral ischemia without reperfusion, 4, 16, 24, 36, 48, and 72 hrs post IRI). This dataset also includes IRI at 48 hrs and 72 hrs in Azin1 A-to-I locked and Azin1 A-to-I uneditable mice.