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Integrative Omics Reveals Subtle Molecular Perturbations Following Ischemic Conditioning in a Porcine Kidney Transplant Model

ABSTRACT: Integrative Omics Reveals Subtle Molecular Perturbations Following Ischemic Conditioning in a Porcine Kidney Transplant Model

PROVIDER: PRJEB47176 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6559211.fastq.gz	Fastqsanger.gz
	ERR6559211_1.fastq.gz	Fastqsanger.gz
	ERR6559211_2.fastq.gz	Fastqsanger.gz
	ERR6559212.fastq.gz	Fastqsanger.gz
	ERR6559212_1.fastq.gz	Fastqsanger.gz

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Integrative Omics Reveals Subtle Molecular Perturbations Following Ischemic Conditioning in a Porcine Kidney Transplant Model

Project description:Background: Remote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the Ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls. Methods: Kidney pairs (n = 8+8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One of the two kidney recipients in each pair was subjected to RIC prior to kidney graft reperfusion, while the other served as non-RIC control. We designed a modern integrative Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC. Results: In kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, which was mirrored at the proteome level. In particular, we noted that RIC resulted in suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in kidney tissues was detected at the protein level, which may be in response to muscle tissue damage and/or fibrosis. Conclusions: Our data identifies subtle molecular phenotypes in porcine kidneys following RIC and this knowledge could potentially aid optimisation of remote ischaemia protocols in renal transplantation.

2021-09-04 | E-MTAB-10872 | biostudies-arrayexpress

Transplant Model Ischemic Conditioning Causes Tissue Leakage and Suppressed Inflammation in a Porcine Kidney

Project description:Background: Remote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the Ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls. Methods: Kidney pairs (n = 8+8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One kidney in each pair was subjected to RIC prior to reperfusion, while the other served as non-RIC control. We designed an advanced integrative -Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC. Results: In kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, but more pronounced effects at the proteome level. In particular, we noted that RIC resulted in response suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in RIC tissues was detected at the protein level, which may result in response to muscle tissue damage and/or fibrosis. Conclusions: Our data identifies subtle molecular phenotypes in porcine kidneys subjected to RIC which could aid further optimisation of remote ischaemia protocols in renal transplantation.

2022-04-04 | PXD025273 | Pride

Integrative omics reveals subtle molecular perturbations following ischemic conditioning in a porcine kidney transplant model.

Project description:BackgroundRemote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls.MethodsKidney pairs (n = 8 + 8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One of the two kidney recipients in each pair was subjected to RIC prior to kidney graft reperfusion, while the other served as non-RIC control. We designed an integrative Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC.ResultsIn kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, which was mirrored at the proteome level. In particular, we noted that RIC resulted in suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in kidney tissues was detected at the protein level, which may be in response to muscle tissue damage and/or fibrosis. However, the majority of these protein changes did not reach significance (p < 0.05).ConclusionsOur data identifies subtle molecular phenotypes in porcine kidneys following RIC, and this knowledge could potentially aid optimization of remote ischemic conditioning protocols in renal transplantation.

| S-EPMC8903695 | biostudies-literature

Pre-transplant conditioning propagates selective loss of host Helios+/Nrp1+ Treg in aHSCT

Project description:Comparative analysis of four murine Treg subsets differentially affected by pre-transplant conditioning and acute gastrointestinal GvHD following allogeneic hematopoietic stem cell transplantation.

2023-03-27 | GSE227929 | GEO

Expression data from plasma exosomal microRNA of rats with remote ischemic conditioning and normal controls

Project description:Remote ischemic conditioning (RIC) is a safely therapeutic strategy for a variety of ischemic diseases, with efficiency comparable to the classic in-situ ischemic methods. Recent evidence has shown that RIC could alter the content of circulating exosomes. microRNAs involves in numerous functionally different biological and physiological processes. The aim of this study is to identify the differentially expressed exosomal microRNAs in rat plasma with RIC and to further explore the functions in ischemic heart diseases. Five RIC rats and 5 control rats were enrolled in this study. We used microarray analysis to identify miRNA expression in their plasma exosomes.

2022-04-01 | GSE198747 | GEO

Remote ischemic conditioning–induced shift from a vulnerable to a tolerant penumbra: a proteomic perspective

Project description:The animals were subjected to focal cerebral ischemia using the filament model without or with post-ischemic remote conditioning. The neurological deficits in animals were assessed and brain infarct volumes were determined. Comparative proteomics was done. Selected candidate proteins were validated by western blotting and immunohistochemistry. Additionally neurodegeneration was assesed.

2025-05-18 | PXD061081 | Pride

Proteomic analysis identifies plasma correlates of remote ischemic conditioning in the context of experimental traumatic brain injury

Project description:Remote ischemic conditioning (RIC) treatment has been shown to modify levels of traumatic brain injury (TBI) pathology related proteins, however, the mechanism is not widely understood. This study utilized LC-MS/MS to identify protein biomarkers of RIC treatment after TBI in mouse models.

2021-06-03 | PXD020420 | Pride

Conditioning-1

Project description:Conditioning-1

| PRJNA1074489 | ENA

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Project description:Conditioning-1

| PRJNA1074490 | ENA

Pre-transplant conditioning propagates selective loss of host Helios+/Nrp1+ Treg in aHSCT

Project description:Pre-transplant conditioning propagates selective loss of host Helios+/Nrp1+ Treg in aHSCT

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