Sus scrofa
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA304600 | ENA |
REPOSITORIES: ENA
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Project description:Lung ischemia-reperfusion (I/R) injury remains one of the common complications after various cardiopulmonary surgeries. I-R injury represents one potentially maladaptive response of the innate immune system which is featured by an exacerbated sterile inflammatory response triggered by tissue damage. Thus, understanding the key components and processes involved in sterile inflammation during lung I-R injury is critical to alter care and extend survival for patients with acute lung injury. We constructed a minipig surgical model of transient unilateral left pulmonary artery occlusion without bronchial involvement to create ventilated lung I-R injury. Lung tissues from minipig with sham operation (one sample), left side lung tissues (the operated side)(one sample) and right side lung tissues (the non-operated side)(one sample) from minipig with lung ischemia-reperfusion were submitted for gene expression array analysis.
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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.
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Project description:To examine the age-related vulnerability to lung ischemia reperfusion injury, pulmonary gene expression profiles after lung ischemia reperfusion were compared between young and old mice.
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Project description:Primary graft dysfunction (PGD), which is caused primarily by ischemia–reperfusion injury (IRI), is a major obstacle in lung transplantation. Here, we developed an orthotopic, single-lung transplant pig model to simulate prolonged cold IRI. After 24 hours of cold ischemia and 8 hours of warm reperfusion, the transplanted lung exhibited severe allograft injury. Subsequent single-cell RNA sequencing (scRNA-seq) revealed significant changes in alveolar macrophages after IRI, with prominently enriched ferroptosis pathways. Transmission electron microscopy (TEM) confirmed characteristic ferroptosis changes in lung macrophages, and decreased GPX4 expression in macrophages indicated increased susceptibility to ferroptosis. Overall, our pig orthotopic left lung transplant model effectively simulates IRI after transplantation, which offers a valuable platform for more detailed investigations of early reperfusion injury to pulmonary grafts. Moreover, we preliminarily demonstrated the importance of macrophage ferroptosis in IRI, suggesting that inhibiting macrophage ferroptosis may be a promising therapeutic strategy for lung IRI.
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