scholarly journals Conditioned Medium from Human Amnion-Derived Mesenchymal Stromal/Stem Cells Attenuating the Effects of Cold Ischemia-Reperfusion Injury in an In Vitro Model Using Human Alveolar Epithelial Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 510
Author(s):  
Vitale Miceli ◽  
Alessandro Bertani ◽  
Cinzia Maria Chinnici ◽  
Matteo Bulati ◽  
Mariangela Pampalone ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Alveolar Epithelial Cells ◽  
Cold Ischemia ◽  
Human Amnion ◽  
Alveolar Epithelial ◽  
Vitro Model

The clinical results of lung transplantation (LTx) are still less favorable than other solid organ transplants in both the early and long term. The fragility of the lungs limits the procurement rate and can favor the occurrence of ischemia-reperfusion injury (IRI). Ex vivo lung perfusion (EVLP) with Steen SolutionTM (SS) aims to address problems, and the implementation of EVLP to alleviate the activation of IRI-mediated processes has been achieved using mesenchymal stromal/stem cell (MSC)-based treatments. In this study, we investigated the paracrine effects of human amnion-derived MSCs (hAMSCs) in an in vitro model of lung IRI that includes cold ischemia and normothermic EVLP. We found that SS enriched by a hAMSC-conditioned medium (hAMSC-CM) preserved the viability and delayed the apoptosis of alveolar epithelial cells (A549) through the downregulation of inflammatory factors and the upregulation of antiapoptotic factors. These effects were more evident using the CM of 3D hAMSC cultures, which contained an increased amount of immunosuppressive and growth factors compared to both 2D cultures and encapsulated-hAMSCs. To conclude, we demonstrated an in vitro model of lung IRI and provided evidence that a hAMSC-CM attenuated IRI effects by improving the efficacy of EVLP, leading to strategies for a potential implementation of this technique.

Novel In Vitro Model For Studying Hepatic Ischemia-Reperfusion Injury Using Liver Cubes

2011 ◽  
Vol 165 (2) ◽  
pp. 281-282
Author(s):  
B.J. DuBray ◽  
K.D. Conzen ◽  
G.A. Upadhya ◽  
P. Balachandran ◽  
J. Jia ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Vitro Model ◽  
Hepatic Ischemia Reperfusion

scholarly journals Novel in vitro model for studying hepatic ischemia-reperfusion injury using liver cubes

Surgery ◽  
2012 ◽  
Vol 152 (2) ◽  
pp. 247-253
Author(s):  
Bernard J. DuBray ◽  
Kendra D. Conzen ◽  
Gundumi A. Upadhya ◽  
Parvathi Balachandran ◽  
Jianluo Jia ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Vitro Model ◽  
Hepatic Ischemia Reperfusion

Hydrogen Sulfide Protects Against Ischemia-Reperfusion Injury in an In Vitro Model of Cutaneous Tissue Transplantation

2010 ◽  
Vol 159 (1) ◽  
pp. 451-455 ◽  
Author(s):  
Peter W. Henderson ◽  
Sunil P. Singh ◽  
Daniel Belkin ◽  
Vamsi Nagineni ◽  
Andrew L. Weinstein ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Tissue Transplantation ◽  
Cutaneous Tissue ◽  
Vitro Model

scholarly journals Adenosine and inosine exert cytoprotective effects in an in vitro model of liver ischemia-reperfusion injury

2012 ◽  
Vol 31 (2) ◽  
pp. 437-446 ◽  
Author(s):  
KATALIN MÓDIS ◽  
DOMOKOS GERŐ ◽  
RITA STANGL ◽  
OLIVÉR ROSERO ◽  
ATTILA SZIJÁRTÓ ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Liver Ischemia ◽  
Vitro Model

scholarly journals Transplantation-Induced Ischemia-Reperfusion Injury Modulates Antigen Presentation by Donor Renal CD11c+F4/80+ Macrophages through IL-1R8 Regulation

2020 ◽  
Vol 31 (3) ◽  
pp. 517-531 ◽  
Author(s):  
Sistiana Aiello ◽  
Manuel Alfredo Podestà ◽  
Pamela Y. Rodriguez-Ordonez ◽  
Francesca Pezzuto ◽  
Nadia Azzollini ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Antigen Presentation ◽  
Kidney Transplant ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cold Ischemia ◽  
Reversible Ischemia ◽  
Antigen Presenting

BackgroundIn donor kidneys subjected to ischemia-reperfusion injury during kidney transplant, phagocytes coexpressing the F4/80 and CD11c molecules mediate proinflammatory responses and trigger adaptive immunity in transplantation through antigen presentation. After injury, however, resident renal macrophages coexpressing these surface markers acquire a proreparative phenotype, which is pivotal in controlling inflammation and fibrosis. No data are currently available regarding the effects of transplant-induced ischemia-reperfusion injury on the ability of donor-derived resident renal macrophages to act as professional antigen-presenting cells.MethodsWe evaluated the phenotype and function of intragraft CD11c+F4/80+ renal macrophages after cold ischemia. We also assessed the modifications of donor renal macrophages after reversible ischemia-reperfusion injury in a mouse model of congeneic renal transplantation. To investigate the role played by IL-1R8, we conducted in vitro and in vivo studies comparing cells and grafts from wild-type and IL-R8–deficient donors.ResultsCold ischemia and reversible ischemia-reperfusion injury dampened antigen presentation by renal macrophages, skewed their polarization toward the M2 phenotype, and increased surface expression of IL-1R8, diminishing activation mediated by toll-like receptor 4. Ischemic IL-1R8–deficient donor renal macrophages acquired an M1 phenotype, effectively induced IFNγ and IL-17 responses, and failed to orchestrate tissue repair, resulting in severe graft fibrosis and aberrant humoral immune responses.ConclusionsIL-1R8 is a key regulator of donor renal macrophage functions after ischemia-reperfusion injury, crucial to guiding the phenotype and antigen-presenting role of these cells. It may therefore represent an intriguing pathway to explore with respect to modulating responses against autoantigens and alloantigens after kidney transplant.

scholarly journals Autophagy Decreases Alveolar Epithelial Cell Injury by Suppressing the NF-κB Signaling Pathway and Regulating the Release of Inflammatory Mediators

2018 ◽  
Author(s):  
Tao Fan ◽  
Shuo Yang ◽  
Zhixin Huang ◽  
Wei Wang ◽  
Shize Pan ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Alveolar Epithelial Cell ◽  
Ischemia Reperfusion ◽  
Left Lung ◽  
Alveolar Epithelial ◽  
Group Blocking

AbstractTo research the impact of autophagy on alveolar epithelial cell inflammation and its possible mechanism in early stages of hypoxia, we established a cell hypoxia-reoxygenation model and orthotopic left lung ischemia-reperfusion model. Rat alveolar epithelial cells stably expressing GFP-LC3 were treated with an autophagy inhibitor (3-methyladenine, 3-MA) or autophagy promoter (rapamycin), followed by hypoxia-reoxygenation treatment at 2, 4 and 6h in vitro. In vivo, twenty-four male Sprague-Dawley rats were randomly divided into four groups (model group: no blocking of hilum in the left lung; control group: blocking of hilum in the left lung for 1h with DMSO lavage; 3-MA group: blocking of hilum in the left lung for 1h with 100ml/kg of 3-MA (5μmol/L) solution lavage; rapamycin group: blocking of hilum in the left lung for 1h with 100ml/kg of rapamycin (250nmol/L) solution lavage) to establish an orthotopic left lung ischemia model. This study demonstrated that rapamycin significantly suppressed the NF-κB signaling pathway, restrained the expression of pro-inflammatory factors. A contrary result was confirmed by 3-MA pretreatment. These findings indicate that autophagy reduces ischemia-reperfusion injury by repressing inflammatory signaling pathways in the early stage of hypoxia in vitro and in vivo. This could be a new protective method for lung ischemia-reperfusion injury.

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