scholarly journals Extraction of green fluorescent protein labelled Mesenchymal Stromal Cells to investigate their mechanisms of action on Ischemia- Reperfusion Injury in a rat kidney transplant model.

Author(s):  
Natalie Vallant
2014 ◽  
Vol 98 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Yiing Lin ◽  
Pamela T. Manning ◽  
Jianluo Jia ◽  
Joseph P. Gaut ◽  
Zhenyu Xiao ◽  
...  

Author(s):  
Anne-Emilie Declèves ◽  
Nathalie Caron ◽  
Denis Nonclercq ◽  
Alexandre Legrand ◽  
Gérard Toubeau ◽  
...  

2005 ◽  
Vol 67 (3) ◽  
pp. 1142-1151 ◽  
Author(s):  
Natalie Serkova ◽  
T. Florian Fuller ◽  
Jost Klawitter ◽  
Chris E. Freise ◽  
Claus U. Niemann

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Di Gu ◽  
Xiangyu Zou ◽  
Guanqun Ju ◽  
Guangyuan Zhang ◽  
Erdun Bao ◽  
...  

Background. The immoderation of mitochondrial fission is one of the main contributors in ischemia reperfusion injury (IRI) and mesenchymal stromal cells (MSCs) derived extracellular vesicles have been regarded as a potential therapy method. Here, we hypothesized that extracellular vesicles (EVs) derived from human Wharton Jelly mesenchymal stromal cells (hWJMSCs) ameliorate acute renal IRI by inhibiting mitochondrial fission through miR-30b/c/d.Methods. EVs isolated from the condition medium of MCS were injected intravenously in rats immediately after monolateral nephrectomy and renal pedicle occlusion for 45 minutes. Animals were sacrificed at 24 h after reperfusion and samples were collected. MitoTracker Red staining was used to see the morphology of the mitochondria. The expression of DRP1 was measured by western blot. miR-30 in EVs and rat tubular epithelial cells was assessed by qRT-PCR. Apoptosis pathway was identified by immunostaining.Results. We found that the expression of miR-30 in injured kidney tissues was declined and mitochondrial dynamics turned to fission. But they were both restored in EVs group in parallel with reduced cell apoptosis. What is more, when the miR-30 antagomirs were used to reduce the miRNA levels, all the related effects of EVs reduced remarkably.Conclusion. A single administration of hWJMSC-EVs could protect the kidney from IRI by inhibition of mitochondrial fission via miR-30.


2007 ◽  
Vol 292 (2) ◽  
pp. F888-F894 ◽  
Author(s):  
Kristin Kirkby ◽  
Chris Baylis ◽  
Anupam Agarwal ◽  
Byron Croker ◽  
Linda Archer ◽  
...  

Exogenous bilirubin (BR) substitutes for the protective effects of heme oxygenase (HO) in several organ systems. Our objective was to investigate the effects of exogenous BR in an in vivo model of ischemia-reperfusion injury (IRI) in the rat kidney. Four groups of male Sprague-Dawley rats were anesthetized using isoflurane in oxygen and treated with 1) 5 mg/kg intravenous (iv) BR, 1 h before ischemia and 6-h reperfusion; 2) vehicle 1 h before ischemia and 6-h reperfusion; 3) 20 mg/kg iv BR, 1 h before and during ischemia; and 4) vehicle 1 h before and during ischemia. Bilateral renal clamping (30 min) was followed by 6-h reperfusion. Infusion of 5 mg/kg iv BR achieved target levels in the serum at 6 h postischemia (31 ± 9 μmol/l). Infusion of 20 mg/kg BR reached 50 ± 22 μmol/l at the end of ischemia, and a significant improvement was seen in serum creatinine at 6 h (1.07 ± 28 vs. 1.38 ± 0.18 mg/dl, P = 0.043). Glomerular filtration rate, estimated renal plasma flow, fractional excretion of electrolytes, and renal vascular resistance were not significantly improved in BR-treated groups. Histological grading demonstrated a trend toward preservation of cortical proximal tubules in rats receiving 20 mg/kg iv BR compared with control; however, neither BR dose provided protection against injury to the renal medulla. At the doses administered, iv BR did not provide complete protection against IRI in vivo. Combined supplementation of both BR and carbon monoxide may be required to preserve renal blood flow and adequately substitute for the protective effects of HO in vivo.


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