Protection of Sinusoidal Endothelial Cells Against Storage/Reperfusion Injury by Prostaglandin E2 Derived From Kupffer Cells1

Arai, Masahiro; Peng, Xing-Xi; Currin, Robert T.; Thurman, Ronald G.; Lemasters, John J.

doi:10.1097/00007890-199908150-00017

Cited by 39 publications

(31 citation statements)

References 32 publications

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“…These observations together with previous reports suggest that arachidonic acid metabolism may be involved not only in the kidney but also in the liver during postischemic reperfusion. Supporting this, prostaglandins and synthetic prostaglandin analogs have shown cytoprotective effects on hepatocytes in experimental models of ischemia-reperfusion liver injury and treatment with prostaglandins is reported to improve graft function after rat liver transplants (10). In addition, we found that the mRNA expression of CYP27, the sterol 27-hydroxylase, which is a ratelimiting enzyme for bile acid synthesis, was decreased following ischemia-reperfusion.…”

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confidence: 59%

Monitoring Expression of Cytochrome P450 Genes During Postischemic Rat Liver Reperfusion Using DNA Microarrays

et al. 2005

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Abstract. We investigated the expression of 50 cytochrome P450 (CYP) genes in the postischemic reperfused rat liver using a DNA microarray. Thirteen CYPs showed absent expression in all experiments and 2 CYPs were induced by pentobarbital, which was used as an anesthetic. Eight of the remaining 35 CYPs showed significantly decreased expression following ischemiareperfusion. Monitoring CYP expression may be a powerful approach for elucidation of pathways regulating drug metabolism that may be involved in postischemic reperfusion liver injury.

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confidence: 59%

Monitoring Expression of Cytochrome P450 Genes During Postischemic Rat Liver Reperfusion Using DNA Microarrays

et al. 2005

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“…34,35 Kupffer-cell activation before storage may affect sinusoidal endothelial-cell injury after storage and reperfusion. 36 However, whole-liver ischemic preconditioning produced nearly the same protection to sinusoidal endothelial cells as half-liver preconditioning.…”

Section: Discussionmentioning

confidence: 99%

Ischemic preconditioning of rat livers against cold storage-reperfusion injury: Role of nonparenchymal cells and the phenomenon of heterologous preconditioning

2001

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Brief periods of ischemia followed by reperfusion render tissues resistant against subsequent prolonged ischemia, a phenomenon called ischemic preconditioning. The effect of ischemic preconditioning on liver transplantation was investigated in relation to sinusoidal endothelial cell injury and Kupffer-cell activation, which are prominent features of storage and reperfusion injury leading to liver graft failure. Rat livers were preconditioned by 5 or 10 minutes of ischemia and 5 minutes of reperfusion and stored in University of Wisconsin (UW) solution for 30 hours. Livers were then reperfused for 15 minutes with physiological buffer containing trypan blue. Under these conditions, injury occurs predominantly to sinusoidal endothelial cells, reflected by trypan blue staining of nonparenchymal cells in histological sections. Ischemic preconditioning decreased nonparenchymal cell killing by more than 50%. When half the liver was preconditioned, sinusoidal endothelial cells were also protected in the contralateral half. Other stored livers were reperfused with nitroblue tetrazolium, which is converted to insoluble formazan by superoxide radicals. Ischemic preconditioning decreased the intensity of formazan deposition over Kupffer cells. Finally, stored livers were transplanted into nontreated rats. Ischemic preconditioning improved recipient long-term survival after 30 hours of cold ischemic storage in UW solution from 30% to 80% and decreased serum tumor necrosis factor-␣ levels in posthepatic blood 4 hours postoperatively from 98 to 54 pg/mL. In conclusion, ischemic preconditioning protects sinusoidal endothelial cells and suppresses Kupffer-cell activation after storage and reperfusion. As a result, graft survival improves after liver transplantation. Moreover, ischemia to half the liver confers protection to the other half. Such heterologous preconditioning provides a new means to protect liver tissue against ischemia-reperfusion injury without imposing ischemia on the target tissue. (Liver Transpl 2001;7:292-299.)

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“…Other constituents could trigger the EE sensor function through the EE-myocardial auto-and paracrine signaling pathways or glomerular epithelial cells in the kidney (31), alveolar epithelial cells in the lungs, or myofiber cells in skeletal muscle are likely to be important but have scarcely been studied. 14 In some animal species, such as the cod family (Gadidae), the endocardial endothelium has evolved to display a third level of decision making within the endothelial system. Through a well-developed scavenger-receptor-mediated endocytosis, the cod EE cells are most effective in clearing and degrading macromolecular waste products of both physiological and pathophysiological processes from the blood (546).…”

Section: The Endothelial System: Conjectural Role Of Cardiac Endotmentioning

confidence: 99%

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

Brutsaert

2003

Physiological Reviews

613

544

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Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.

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Protection of Sinusoidal Endothelial Cells Against Storage/Reperfusion Injury by Prostaglandin E2 Derived From Kupffer Cells1

Abstract: PGE2 derived from LPS-stimulated Kupffer cells protects sinusoidal endothelial cells against storage/reperfusion injury. Unlike LPS, PGE2 improves graft function after liver transplants. Thus, donor preconditioning with PGE2 may be beneficial in liver transplants.

Cited by 39 publications

References 32 publications

Monitoring Expression of Cytochrome P450 Genes During Postischemic Rat Liver Reperfusion Using DNA Microarrays

Monitoring Expression of Cytochrome P450 Genes During Postischemic Rat Liver Reperfusion Using DNA Microarrays

Ischemic preconditioning of rat livers against cold storage-reperfusion injury: Role of nonparenchymal cells and the phenomenon of heterologous preconditioning

Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

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