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: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.
Project description:Renal ischemia reperfusion injury (I/R) has great clinical relevance and many treatments and hospitalizations are associated with this pathological process. Animal models are widely used in the development of kidney I/R studies and numerous papers have been published in this field in recent years suggesting that the nature of the animal species used in these models can lead to a different response to ischemic insult. The Brown Norway (BN) rat strain is known to show endogenous resistance to the ischemic process and several studies have sought to identify the cell mechanism present in this resistance. Despite of all the previously reported works, little is know about the genetic response of BN in front of ischemic insult. By means of a microarray comparative genetic study between BN and the ischemia susceptible rat strain Sprague Dawley (SD), the present work determine the genetic response to the I/R process in both rat strains and the genes that are differentially expressed during the I/R process and link them with some of the main cytoprotective processes responsible for the endogenous resistance to renal ischemic injury in BN rats. The following experimental groups for BN and SD rats (n=3 per group) were studied: Group 1: Control (C): Animals subjected to identical maneuvers as the I/R group except that the renal pedicles were not clamped. Group 2: Ischemia/Reperfusion (I/R): Animals were subjected to 45 min of bilateral ischemia and 24 h of reperfusion. Gene expression profiles were obtained from control and I/R groups in the two rat strains in three biological replicates, resulting in 12 hybridizations from 2 groups × 2 strains × 3biological replicates. To evaluate the technical reliability of microarrays, replicate microarrays were performed on several RNA samples. In total, 12 hybridizations were performed for this study.