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Expression of Human Lung Before and After Transplantation

ABSTRACT: Ischemia reperfusion induced injury contributes to poor lung transplant outcomes. We used microarrays 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)

ORGANISM(S): Homo sapiens

PROVIDER: GSE127003 | GEO | 2020/06/22

REPOSITORIES: GEO

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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

Expression of Human Lung Before and After Ex Vivo Lung Perfusion

Project description:Ex vivo lung perfusion restores normothermia, ventilation and circulation to donor lungs, typically after a period of cold ischemia. This allows donor lungs to be evaluated prior to transplantation. We used microarrays to study the biological response of human lungs to Ex Vivo Lung Perfusion. Samples were collected from donor lungs at Toronto General Hospital. Lungs were donation after brain death (DBD)

2020-06-22 | GSE127055 | 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

Lung transplantation-induced cold ischemia–reperfusion injury in the murine lung

Project description:Cold ischemia-reperfusion induced injury contributes to poor lung transplant outcomes. We used transcriptome sequencing to study the biological response of mouse lungs to the cold ischemia-reperfusion process. Mouse orthotopic left LTx was performed with standard cuff techniques. Briefly, the donor lungs were recovered after being flushed with 10ml low potassium dextran (LPD) solution and inflated with 50% oxygen. Cold ischemia was induced by storing donor lungs in 20ml LPD at 4°C for 24 hours. Then, the left donor lung was cuffed and implanted into recipients within 45 minutes. After the 4-hour reperfusion, the recipient mice were sacrificed and the transplanted lungs were collected.

2023-01-20 | GSE222957 | GEO

Mapping Ischemia Reperfusion Inflammatory Responses in Human Lung Transplantation at Single-Cell Resolution

Project description:Ischemia reperfusion (IR) is an unavoidable step of organ transplantation. IR-induced injury constrains the number of donor lungs used for transplant. Here we performed longitudinal single-cell RNA sequencing (scRNA-seq) from human lungs of six individuals who underwent lung transplantation. Lung biopsies were collected after cold preservation and 2-hour reperfusion for each individual resulting in the profiling of 108,613 cells in total.

2024-10-12 | GSE220797 | GEO

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

2009-11-12 | GSE18995 | GEO

Macrophage infiltration induced by donor hypovolemia protects against severe primary graft dysfunction in mouse lung transplantation

Project description:BACKGROUND: Hypovolemia is common in lung donors before or after brain death. However, its impact on primary graft function (PGD) remains obscure. METHODS: A clinically relevant two-hit model of PGD was established by integrating hypovolemic shock (HS) and cold ischemia-reperfusion in a mouse model of orthotopic lung transplantation (LTx) from C57BL/6 to Balb/c. At -48 hours, HS was induced to donor by withdrawal of blood from femoral artery and keeping the mean arterial pressure at 15±5 mmHg for 4 h. At -24 hours, donor lungs were retrieved from mice with or without HS and stored at 0ºC until transplantation. CD11b-DTR mice were used as donor and treated with Diphtheria Toxin (DT) to deplete graft-infiltrating macrophages. RESULTS: HS mainly caused macrophage-predominant infiltration around pulmonary artery injury systemic inflammatory response, but little impairment of lung function even if in combination with cold ischemia-reperfusion. Transcriptional profiling showed HS pretreatment increased pulmonary damage and alveolar remodeling but ameliorated inflammatory infiltration when compared to one-hit model of 12 hours cold ischemia-reperfusion injury. The allografts with donor DT-treatment one day ahead of HS showed injury and dysfunction at donation and worsened further at 24 hours reperfusion, whereas the allografts with recipient DT-treatment immediately after transplantation showed similar function and histology to the control treated with saline. CONCLUSION: Donor hypovolemia causes pulmonary artery injury and infiltration but has little impact on allograft function, even in combination with 24 h cold ischemia. Graft-infiltrating macrophages are critical in protecting graft from HS-induced injury and cold ischemia-reperfusion injury.

2022-03-30 | GSE156322 | GEO

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

Gene Expression Changes due to Rat Lung Ischemia-Reperfusion Injury

Project description:Ischemia-reperfusion injury (IRI) is a major cause of morbidity and mortality following conventional lung transplantation and warm ischemia may limit success of transplanting lungs from non-heart-beating donors. We sought to determine alterations in gene expression in rat lung tissue subjected to warm ischemia in vivo followed by reperfusion. Keywords: time course

2019-04-30 | GSE9634 | GEO

Cardiac-dead mouse lungs may remain transplantable at 37ºC for 4 hours if gas exchange is preserved

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.

2022-03-30 | GSE154939 | GEO

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