ABSTRACT: MiRNA expression profile in human CD34+/CD105- cells derived from the renal artery subsequent to long warm ischemia compared short warm ischemia
Project description:MiRNA regulate the maintenance, differentiation and function of stem cells and progenitor cells. miRNA expression of progenitor cells located in the adventital layer of arterial vessels has not been characterized in either animal or human models. Further it is unknown if local arterial miRNA expression profiles change after injury of end organs supplied blood by these arterial conduits. CD34+/CD105- cells were extracted and analyzed for changes in miRNA expression after kidney specific ischemic injury. CD34+/CD105- cells were isolated from renal artery after short warm ischemic time in living donor kidney explants and long warm ischemic time following radical nephrectomy for renal cell cancer
Project description:MiRNA regulate the maintenance, differentiation and function of stem cells and progenitor cells. miRNA expression of progenitor cells located in the adventital layer of arterial vessels has not been characterized in either animal or human models. Further it is unknown if local arterial miRNA expression profiles change after injury of end organs supplied blood by these arterial conduits. CD34+/CD105- cells were extracted and analyzed for changes in miRNA expression after kidney specific ischemic injury. CD34+/CD105- cells were isolated from mouse renal artery after microvascular clamping of renal arteries bilaterally
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:Transcriptome analysis was done after warm renal ischemia-reperfusion injury (IRI) in a rat model. Earlier studies have shown a protective effect of prior unilateral nephrectomy (UNx) against IRI in the remaining, contralateral kidney compared to a non-neprectomized control group. We aimed at identifying the underlying molecular mechanisms. We used the Affymetrix Clariom D array (formerly known as RTA 1.0 st.) Array data was processed in the Affymetrix Console Software.
Project description:Despite a potentially huge number, uncontrolled donation after circulatory death contributed little to alleviating donor lung shortage due to rapidly progressive warm ischemia. Many methods have been studied in animals, but the tolerable warm ischemic time (WIT) remains less than 90 minutes. Using a refined mouse model of pulmonary artery ligation (PAL), we firstly determined the maximum tolerable WIT. 4-hour PAL caused mild lung infiltration without dysfunction upon reperfusion, whereas 5-hour PAL triggered arterial endothelium injury and more significant infiltration with dysfunction. Transcriptional profiling showed a myeloid-dominant inflammation with mild injury in 4-hour PAL. The maximum WIT was then adapted in a clinically relevant scenario. Donor mice died of circulatory arrest without heparization and remained at 37ºC for 4 hours, followed by isogenic transplantation. As observed in 4-hour PAL, nonhypoxic warm ischemia-reperfusion hardly affected graft function and histology, no matter if warm ischemic lung preserved gas exchange by spontaneously breathing or by postmortem protective ventilation. If the dead donors were left untouched, however, the grafted lungs suffered severe hypoxic warm ischemia-reperfusion injury, varying from partially aerated totally lost. Taken together, the retrieval time can be extended to 4 hours at 37ºC by preventing cardiac-dead donor lung hypoxia.
Project description:Normothermic ex-vivo kidney perfusion (NEVKP) has demonstrated superior outcomes for donation-after-cardiovascular death (DCD) grafts compared to static cold storage (SCS). To determine the mechanisms responsible for this, we performed an unbiased genome-wide microarray analysis. Kidneys from 30kg-Yorkshire pigs were subjected to 30min of warm ischemia followed by 8hrs of NEVKP or SCS, or no storage (NS), prior to auto-transplantation. mRNA expression was analyzed on POD3 renal biopsies.
Project description:TLR4/NF-κB signaling plays a central mediator in response to danger signals released in the muscle ischemia-reperfusion injury (IRI). This study was designed to profile TLR4/NF-κB-responsive microRNAs (miRNAs) in the skeletal muscles following IRI. Following 2 h of ischemia and subsequent reperfusion for indicated times (0 h, 4 h, 1 d, and 7 d) of the isolated thigh skeletal muscles based on femoral artery perfusion of C57BL/6, Tlr4–/–, and NF-κB–/–mice, the muscle specimens were analyzed with an miRNA array to detect the TLR4/NF-κB-responsive miRNAs.
Project description:Purpose: The goals of this study are to dessect the molecular signature of CD31+CD34+HEPs with different expression of CD105 ,and to explore the regulators such as signaling and transcription factors of CD105+ cells' generation. Methods: mRNA profiles of HEPs samples collected at day4 of hematopoietic differentiation were generated by deep sequencing using Illumina HiSeq 2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Conclusions: The CD31+CD34+CD105-HEPs possess hematopoietic potential whereas the CD31+CD34+CD105+HEPs possess endothelial potential. In addition, the generation of CD105+cells were regulated by TGFbeta signaling and ETS1.
