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Cellular Recovery After Prolonged Warm Ischemia of the Whole Body

ABSTRACT: Here we use single-cell transcriptome analysis in healthy and varying ischemic conditions across 4 vital organs such as brain (hippocampus), heart, liver and kidney to better understand the changes occurring following the cessation of the blood flow. Furthermore, we use these datasets as references to characterize changes on the single-cell transcriptome level that are induced by re-introduction of the blood flow to the same organs.

ORGANISM(S): Sus scrofa

PROVIDER: GSE183448 | GEO | 2022/08/03

REPOSITORIES: GEO

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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

2015-04-29 | E-GEOD-68366 | biostudies-arrayexpress

MiRNA expression profile in human CD34+/CD105- cells derived from the renal artery subsequent to long warm ischemia compared short warm ischemia

2015-04-29 | GSE68366 | GEO

Cellular Recovery After Prolonged Warm Ischemia of the Whole Body

Project description:Cellular Recovery After Prolonged Warm Ischemia of the Whole Body

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Factors Associated With Prolonged Warm Ischemia Time Among Deceased Donor Kidney Transplant Recipients.

Project description:Background:Prolonged warm ischemia time (WIT) is associated with graft failure and mortality, however less is known about factors associated with prolonged WIT. Methods:In a cohort of United States deceased donor kidney transplant recipients identified using the Scientific Registry of Transplant Recipients (Jan 2005-Dec 2013), we identified factors associated with prolonged WIT (defined as ? 30 minutes versus 10-30 minutes) using hierarchical multilevel models adjusting for center effect, and WIT as a continuous variable using multiple linear regression of log-transformed data. Results:Among 55 829 patients, potentially modifiable risk factors associated with prolonged WIT included increased recipient body mass index (BMI) (odds ratio [OR], 1.57; 95% confidence interval [CI], 1.44-1.72 for BMI > 35), right donor kidney (OR, 1.14; 95% CI, 1.08-1.19), and a prolonged cold ischemic time (OR, 1.23; 95% CI, 1.13-1.33 for cold ischemia time > 24 hours). Transplanting a right kidney into an obese recipient further prolonged WIT (OR, 1.75; 95% CI, 1.55-1.98; for BMI > 35), increasing overall WIT by 11.0%. There was no correlation between median WIT for a given center and annual center transplant rate (pairwise correlation coefficient, 0.0898). Conclusions:In conclusion, several modifiable factors are associated with prolonged WIT and may represent strategies to improve WIT and subsequent posttransplant outcomes.

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Project description:Insufficient supply of cardiac grafts represents a severe obstacle in heart transplantation. Donation after circulatory death (DCD), in addition to conventional donation after brain death, is one promising option to overcome the organ shortage. However, DCD organs undergo an inevitably longer period of unprotected warm ischemia between circulatory arrest and graft procurement. In this scenario, we aim to improve heart preservation after a warm ischemic period of 20 min by testing different settings of myocardial protective strategies. Pig hearts were collected from a slaughterhouse and assigned to one of the five experimental groups: baseline (BL), cold cardioplegia (CC), cold cardioplegia + adenosine (CC-ADN), normothermic cardioplegia (NtC + CC) or normothermic cardioplegia + cold cardioplegia + adenosine (NtC-ADN + CC). After treatment, tissue biopsies were taken to assess mitochondrial morphology, antioxidant enzyme activity, lipid peroxidation and cytokine and chemokine expressions. NtC + CC treatment significantly prevented mitochondria swelling and mitochondrial cristae loss. Moreover, the antioxidant enzyme activity was lower in this group, as was lipid peroxidation, and the pro-inflammatory chemokine GM-CSF was diminished. Finally, we demonstrated that normothermic cardioplegia preserved mitochondria morphology, thus preventing oxidative stress and the subsequent inflammatory response. Therefore, normothermic cardioplegia is a better approach to preserve the heart after a warm ischemia period, with respect to cold cardioplegia, before transplantation.

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Significant Dysfunction of Kidney Grafts Exposed to Prolonged Warm Ischemia Is Minimized Through Normothermic Ex Vivo Kidney Perfusion.

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Project description:Elastin insufficiency causes globally reduced caliber blood vessels and arterial stiffnesss that contribute to reduction of blood flow to end organs such as the brain. Treatment with minoxidil increases vessel caliber and blood flow.

2018-03-08 | GSE110296 | GEO

GPR174 Knockdown Enhances Blood Flow Recovery in Hindlimb Ischemia Mice Model by Upregulating AREG Expression

Project description:GPR174 Knockdown Enhances Blood Flow Recovery in Hindlimb Ischemia Mice Model by Upregulating AREG Expression

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GPR174 Knockdown Enhances Blood Flow Recovery in Hindlimb Ischemia Mice Model by Upregulating AREG Expression

Project description:Regulatory T cells (Tregs) are critically involved in neovascularization, an important compensatory mechanism in peripheral artery disease (PAD). The contribution of G protein coupled receptor 174 (GPR174), which is a regulator of Treg function and development, in neovascularization remains elusive. Here, we reveal that genetic deletion of GPR174 in Tregs potentiated blood flow recovery in mice after hindlimb ischemia (HLI). GPR174 deficiency upregulates amphiregulin (AREG) expression in Tregs, thereby enhancing endothelial cell functions and reducing pro-inflammatory macrophage polarization and endothelial cell apoptosis. Mechanically, GPR174 regulates AREG expression by inhibiting the nuclear accumulation of early growth response protein 1 (EGR1) via Gαs/cAMP/PKA signal pathway activation. Collectively, these findings demonstrate that GPR174 negatively regulates angiogenesis and vascular remodeling in response to ischemic injury and that GPR174 may be a potential molecular target for therapeutic interventions of ischemic vascular diseases.

2022-10-03 | GSE214684 | GEO

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