Prevention of renal ischemic reperfusion injury using FTY 720 and ICAM-1 antisense oligonucleotides

Ortiz, A.M.; Troncoso, P.; Kahan, Barry D.

doi:10.1016/s0041-1345(03)00374-9

Cited by 20 publications

(12 citation statements)

References 15 publications

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“…S1P markedly promotes lung tissue homeostasis by attenuating I/R lung injury through preventing endothelial cell barrier damage, inhibiting mononuclear cell migration and pulmonary cell apoptosis in transplanted lung grafts following reperfusion. The use of S1P agonists to attenuate ischemic injury in other organs such as kidney and liver has been recently described indicating that targeting signals that modulate lymphocyte trafficking is a potentially effective method to prevent organ injury in the immediate period following transplantation (24)(25)(26)(27). However, these organs are comparably less susceptible to I/R injury suggesting the use of S1P receptor agonists could be an even more effective modality to prevent reperfusion injury to the lung.…”

Section: Discussionmentioning

confidence: 99%

Sphingosine 1-Phosphate Inhibits Ischemia Reperfusion Injury Following Experimental Lung Transplantation

Okazaki

Kreisel

Richardson

et al. 2007

American Journal of Transplantation

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Ischemia reperfusion (I/R) injury following lung transplantation is exacerbated by the destruction of the endothelial cell barrier leading to pulmonary edema and dysregulated activated lymphocyte migration. Sphingosine 1-phosphate (S1P), a G-coupled protein receptor (GPCR) agonist, has been previously shown to promote endothelial cell tight junction formation and prevent monocyte chemotaxis. We asked if S1P treatment could improve pulmonary function and attenuate I/R injury following syngeneic rat lung transplantation. In comparison to vehicle-treated recipients, S1P administered before reperfusion significantly improved recipient oxygenation following transplantation. Improved graft function was associated with reduced inflammatory signaling pathway activation along with attenuated intragraft levels of MIP-2, TNF-a and IL1b . Moreover, S1P-treated recipients had significantly less apoptotic endothelial cells, pulmonary edema and graft accumulation of neutrophils than did vehicletreated recipients. Thus our data show that S1P improves lung tissue homeostasis following reperfusion by enhancing endothelial barrier function and blunting monocytic graft infiltration and inflammation.

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Section: Discussionmentioning

confidence: 99%

Sphingosine 1-Phosphate Inhibits Ischemia Reperfusion Injury Following Experimental Lung Transplantation

Okazaki

Kreisel

Richardson

et al. 2007

American Journal of Transplantation

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“…FTY720 prevents acute rejection without causing renal toxicity [15,16] and could be therefore an exciting candidate for immunosuppression after kidney transplantation. Moreover, FTY720 has been shown to improve kidney recovery after IR in rodents [11][12][13][14].…”

Section: Discussionmentioning

confidence: 99%

“…FTY720 is a new compound with immunomodulatory characteristics that in rodents models of IR provided earlier recovery of renal function and also a lesser degree of acute tubular necrosis and infiltrating leukocytes [11][12][13][14]. In animal models of renal toxicity, FTY720 (1 mg/kg/day) administered during 21 days alone or in association with Cyclosporine (CsA) did not cause significant changes in renal structure and function [15].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of stem cell administration in a model of kidney ischemia-reperfusion injury

Silva

Palma

Cury

et al. 2007

International Immunopharmacology

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“…The etiological factors which lead to ischemic injury have never been selective and are rarely preventable. Two exceptions to this rule are kidney transplantation and renal artery clamping during aortic surgery [2,3,4,5,6,7,8,9]. Furthermore, kidneys harvested from marginal cadaveric donors showed a less favorable outcome which increases the urgency for more efficient preventive strategies against I/R [10].…”

Section: Introductionmentioning

confidence: 99%

Allopurinol and Enalapril Failed to Conserve Urinary NOx and Sodium in Ischemic Acute Renal Failure in Spontaneously Hypertensive Rats

Radović

Miloradović²,

Popović³

et al. 2006

Am J Nephrol

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Background: Ischemia-reperfusion-induced acute renal failure (ARF) is associated with a high mortality in patients with hypertension and with an unfavorable outcome of kidney transplants from marginal donors. Aim: The influence of allopurinol and enalapril on urinary nitrate/nitrite (UNOx), glomerular filtration rate, plasma and urinary sodium, and hemodynamic parameters was examined in spontaneously hypertensive rats (SHR) with ARF. Methods: ARF was induced by right-kidney removal and clamping the left renal artery for 40 min in 50 male 26-week-old SHR weighing 300 ± 23 g. The rats were randomly allocated to five groups: (1) sham operated; (2) ARF; (3) ARF after pretreatment with 40 mg/kg allopurinol; (4) ARF after pretreatment with 40 mg/kg enalapril, and (5) ARF after pretreatment with 40 mg/kg allopurinol and 40 mg/kg enalapril. Creatinine clearance, UNOx (Griess reaction), cardiac output (dye dilution technique), mean arterial blood pressure, and renal blood flow were measured 24 h after reperfusion. Total vascular resistance and renal vascular resistance were calculated and compared between the groups. Results: A nonsignificant decrease was found in both daily UNOx excretion and creatinine clearance when pretreated ARF groups and the ARF group without pretreatment were compared (p > 0.05). Significantly lower plasma sodium values (139.5 ± 4.86 mmol/l) in the allopurinol-pretreated ARF group were found than in the ARF group without pretreatment, in the ARF group pretreated with enalapril, and in the sham SHR group (p = 0.029). The urinary sodium loss was greater in the enalapril-pretreated than in the allopurinol-pretreated ARF group (p = 0.047). Allopurinol and/or enalapril pretreatment decreased total vascular resistance (p = 0.003) in comparison with the sham SHR group. Conclusion: Neither allopurinol nor enalapril nor both were protective against ischemia-reperfusion injury in SHR, nor altered glomerular filtration rate and UNOx in a favorable direction.

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Prevention of renal ischemic reperfusion injury using FTY 720 and ICAM-1 antisense oligonucleotides

Cited by 20 publications

References 15 publications

Sphingosine 1-Phosphate Inhibits Ischemia Reperfusion Injury Following Experimental Lung Transplantation

Sphingosine 1-Phosphate Inhibits Ischemia Reperfusion Injury Following Experimental Lung Transplantation

Evaluation of stem cell administration in a model of kidney ischemia-reperfusion injury

Allopurinol and Enalapril Failed to Conserve Urinary NOx and Sodium in Ischemic Acute Renal Failure in Spontaneously Hypertensive Rats

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