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LncRNA expression profile in hepar tissues of 12h after brain death or matched non-brain death donor liver transplantation

ABSTRACT: LncRNA expression profile in hepar tissues of 12h after brain death or matched non-brain death donor liver transplantation

PROVIDER: PRJNA484774 | ENA |

REPOSITORIES: ENA

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Liver tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

Project description:To determine the circRNA expression profile in hepar tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation, we uesed circRNA microArray analysis form Arraystar to examine the expression of circRNAs and circRNAs in hepar tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

2020-04-10 | GSE119748 | GEO

LncRNA expression profile in hepar tissues of 12h after brain death or matched non-brain death donor liver transplantation

Project description:Brain death donor liver is an important organ source for liver transplantation.The liver injury after brain death donor liver transplantation is serious and the mechanism is unknown.In order to explore the role of lncRNAs and circRNAs expression profile and their biological functions in liver injury after brain death and liver transplantation, lncRNA and mRNA microarray expression profile were tested in the liver after brain death and normal liver transplantation.And this study lays a foundation for future studies on the potential role of lncRNAs in liver injury after brain death donor liver transplantation. To determine the LncRNA expression profile in hepar tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation, we uesed LncRNA microArray analysis form Arraystar to examine the expression of LncRNAs and circRNAs in hepar tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

2021-08-06 | GSE118182 | GEO

Liver tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

Project description:Liver tissues of 12h after brain death donor liver transplantation and matched non-brain death donor liver transplantation.

| PRJNA490174 | ENA

Brain death associated activation of Calpain-Talin axis in donor kidneys underlies podocyte matrix degradation and graft dysfunction in kidney transplantation

Project description:Deceased kidney donation after brain death (DBD) is the main source of transplants, yet these grafts yield inferior transplant outcomes when compared to living donation. In brain death, cerebral injury contributes to systemic biological dysregulation, causing significant cellular stress in donor kidneys that adversely impacts the quality of grafts. Here, we hypothesized that proteolytic processes in DBD kidneys might lead to podocyte damage with subsequent development of post-transplant dysfunction. Using protein topography and migration analysis platform (PROTOMAP), we mapped degradation profiles of cytoskeletal proteins in DBD kidneys. Cytoskeletal proteolytic degradation was further studied by Immunoblotting on a separate cohort of deceased and living donor kidney biopsies. To investigate potential mechanism of kidney cytoskeletal protein degradation, in-vitro human podocytes and ex-vivo precision-cut human kidney slices were employed. We found novel proteolytic profiles of key podocyte cytoskeletal proteins in donor kidneys associated with suboptimal posttransplant function. These were unique to brain-death and were not observed in circulatory-death or living-donor kidneys. Talin-specific protein degradation in DBD kidneys indicated Calpain-1 activation may have a key role in proteolytic processes observed in the dysfunctional kidneys. Investigation of the underlying mechanism suggests that Transforming-Growth Factor-Î² (TGFÎ²) induces Calpain-1 activation, leading to brain-death specific podocyte degradation patterns and dysregulation of actin cytoskeleton; events that were prevented, in-vitro, by Calpain inhibition. Conclusion Our data demonstrate that podocyte protein degradation impacts the quality of DBD kidneys, propose a role of TGFÎ² mediated Calpain-1 proteolytic processing of cytoskeletal Talin-1, suggesting therapeutic opportunities to prevent kidney dysfunction.

2022-08-12 | PXD022074 | Pride

Expression data from donor lungs of cardiac death and brain death donors

2009-11-12 | GSE18995 | GEO

Expression data from donor lungs of cardiac death and brain death donors (re-analysis)

Project description:Ischemia reperfusion induced injury contributes to poor lung transplant outcomes.Microarrays were used to study the biological response of human lungs to the ischemia reperfusion process. Samples were collected from lung transplant cases at Toronto General Hospital. Lungs were donation after brain death (DBD)

2023-09-18 | GSE127242 | GEO

Transcription profiling of lung tissue from cardiac death and brain death donors, both pre and post transplant

Project description:Lung donation after cardiac death (DCD), in contrast to donation after brain death (DBD), is a promising and increasingly common method to help relieve the shortage of donor organs. However, the pathogenetic consequences of retrieved lungs after DCD vs. DBD have not been clarified. We aimed to study the differential gene expression profiles in lungs of DCD and DBD patients. DCD patients were matched with DBD lung transplant cases from a prospectively maintained database. The number of tissue samples included in this study was 6 pre- and 5 post-transplant in DCD and 12 pre- and 12 post-transplant in DBD for a total number of 35 lung tissue samples.

2009-11-11 | E-GEOD-18995 | biostudies-arrayexpress

RNA-seq of perihaematomal and anatomically matched contralateral brain tissue after intracerebral hemorrhage

Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor NRF2, we performed bulk RNA sequencing of perihaematomal and anatomically matched contralateral brain homogenate obtained at autopsy from a cohort of patients who died either within 24h of ICH or between 4-14 days of ICH onset, to investigate the spatiotemporal evolution of this Nrf2 activation.

2024-08-13 | E-MTAB-14323 | biostudies-arrayexpress

Death Receptors DR6 and TROY Regulate Brain Vascular Development

Project description:Signaling events that regulate central nervous system (CNS) angiogenesis and blood-brain barrier (BBB) formation are only beginning to be elucidated. By evaluating the gene expression profile of mouse vasculature, we identified DR6/TNFRSF21 and TROY/TNFRSF19 as regulators of CNS-specific angiogenesis in both zebrafish and mice. Furthermore, these two death receptors interact both genetically and physically and are required for vascular endothelial growth factor (VEGF)-mediated JNK activation and subsequent human brain endothelial sprouting in vitro. Increasing beta-catenin levels in brain endothelium upregulate DR6 and TROY, indicating that these death receptors are downstream target genes of Wnt/beta-catenin signaling, which has been shown to be required for BBB development. These findings define a role for death receptors DR6 and TROY in CNS-specific vascular development. 5 replicates of 3 time points for either brain or liver/lung facs sorted vascaulture. One adult liver/lung replicate was not used as it failed QC

2012-02-15 | E-GEOD-35802 | biostudies-arrayexpress

Haploidentical versus Matched Unrelated versus Matched Sibling Donor Hematopoietic Cell Transplantation with Post-Transplantation Cyclophosphamide.

Project description:With the use of post-transplantation cyclophosphamide (PTCy), the outcomes of mismatched related donor hematopoietic cell transplantation (HCT) are now approaching those of matched donor HCT. Here we compared haploidentical donor HCT versus HLA-matched unrelated donor (MUD) HCT and HLA-identical sibling donor (MSD) HCT in a cohort in which all patients received PTCy for graft-versus-host disease (GVHD) prophylaxis. We included 661 patients (275 haploidentical, 246 MUD, and 140 MSD HCT). The most common diagnoses were acute myelogenous leukemia and myelodysplastic syndrome. In multivariate analysis, the haploidentical group was found to have significantly higher nonrelapse mortality (NRM) (hazard ratio [HR], 3.2; 95% confidence interval [CI], 2 to 4.9; P < .001) and inferior progression-free survival (HR, 1.8; 95% CI, 1.4 to 2.4; P < .001) and overall survival (OS; HR, 2.2; 95% CI, 1.6 to 3; P < .001) compared with the MUD group. Relapse was the most common cause of death in all groups. Among causes of NRM, the haploidentical group had more infection-related deaths and fewer GVHD-related deaths than the other groups. The haploidentical group also had a higher risk of viral and fungal infections, grade ≥3 hemorrhagic cystitis, and cardiovascular toxicities and slower reconstitution of CD4, CD8, and regulatory T cells but faster reconstitution of natural killer cells. In an exploratory analysis, older patients with older donors (>50 years for both) appeared to have particularly high NRM and lower OS in the haploidentical group compared with the other groups. Our data suggest that even with the use of PTCy, the outcomes of haploidentical HCT are inferior to those of HLA-matched donor HCT.

| S-EPMC10152475 | biostudies-literature

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