Protection of transplant-induced renal ischemia-reperfusion injury with carbon monoxide

Neto, João Seda; Nakao, Atsunori; Kimizuka, Kei; Romanosky, Anna Jeanine; Stolz, Donna B.; Uchiyama, Takashi; Nalesnik, Michael A.; Otterbein, Leo E.; Murase, Noriko

doi:10.1152/ajprenal.00158.2004

Cited by 174 publications

(155 citation statements)

References 47 publications

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“…This observation suggests that these compounds are sufficiently concentrated in the kidney to increases local levels of CO in the absence of any decreases in COHb levels. This aspect of these compounds makes them attractive alternatives to CO inhalation therapy, which requires high levels of COHb in the blood to be achieved to be effective (12). We also found that these compounds seem to lose their beneficial qualities when administered after the ischemic episode.…”

Section: Discussionmentioning

confidence: 75%

“…There have been several reports that inhalation of CO can be protective against acute rejection of intestine, lung, and kidney transplants (11,12,23,24). The protective actions of CO inhalation in transplantation are associated with a decrease in inflammation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…One approach has been to use direct CO inhalation therapy at concentrations that increase carboxyhemoglobin levels to 25% after CO inhalation. Recent studies have indicated that CO inhalation therapy is able to protect both intestinal and renal grafts from ischemic damage in experimental models (11,12). However, CO inhalation therapy does have the potential to induce clinical toxicity to achieve the systemic carboxyhemoglobin levels required for therapeutic benefits.…”

mentioning

confidence: 99%

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Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Vera

Henegar²,

Drummond³

et al. 2005

Journal of the American Society of Nephrology

129

105

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Heme oxygenase (HO) induction has been demonstrated to be beneficial in limiting the extent of cellular damage after ischemia-induced acute renal failure (ARF). Because increased HO activity is associated with the production of carbon monoxide (CO) as well as the potent antioxidant bilirubin, it is unclear which of the two is of greater importance in the protective effects of HO induction. The purpose of this study was to determine the protective role of CO alone in ischemia-induced ARF. Bilateral clamping of the renal pedicle for 40 min was associated with a ninefold increase in the levels of plasma creatinine 24 h after reperfusion as compared with normal plasma creatinine levels; however, administration of CO donor compounds tricarbonyldichlororuthenium(II) dimer, ([Ru(CO) 3 Cl 2 ] 2 , 10 mg/kg) or tricarbonylchloro(glycinato)ruthenium(II) ([Ru(CO) 3 Cl(glycinate)], (CORM-3) 1 h before the onset of ischemia significantly decreased the levels of plasma creatinine 24 h after reperfusion as compared with vehicle-treated mice. Surprising, treatment with the CO donors was associated with an increase in HO activity 24 h after ischemia. For determining whether the protective effects of the CO donors were due to CO or HO-1 induction, experiments were performed in which HO was inhibited before administration of the CO donors. Pretreatment with the HO inhibitor had no effect on the level of plasma creatinine 24 h after reperfusion after treatment with the CO donor compounds. These results suggest that CO itself may be protective and limit renal damage in ischemia induced ARF. 16: 950-958, 2005. J Am Soc Nephrol

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Vera

Henegar²,

Drummond³

et al. 2005

Journal of the American Society of Nephrology

129

105

View full text Add to dashboard Cite

show abstract

“…However, few studies examined the role of HO-1 and CO in kidney injury, and the functional role of CO in the context of renal fibrosis has not been previously examined. HO-1 overexpression or CO administration has been shown to protect experimental kidney transplants from ischemia-reperfusion injury (4,30). Moreover, the administration of CO donor compounds, namely carbon monoxide-releasing molecules (CORM-3), protected against cisplatin nephrotoxicity and ischemia-reperfusion-induced renal injury (44,47).…”

Section: Discussionmentioning

confidence: 99%

Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction

Wang¹,

Lee²,

Kwak³

et al. 2008

American Journal of Physiology-Renal Physiology

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Tubulointerstitial fibrosis is a hallmark of chronic progressive kidney disease leading to end-stage renal failure. An endogenous product of heme oxygenase activity, carbon monoxide (CO), has been shown to exert cytoprotection against tissue injury. Here, we explored the effects of exogenous administration of low-dose CO in an in vivo model of renal fibrosis induced by unilateral ureteral obstruction (UUO) and examined whether CO can protect against kidney injury. UUO in mice leads to increased extracellular matrix (ECM) deposition and tubulointerstitial fibrosis within 4 to 7 days. Kidneys of mice exposed to low-dose CO, however, had markedly reduced ECM deposition after UUO. Moreover, low-dose CO treatment inhibited the induction of α-smooth muscle actin (α-SMA) and major ECM proteins, type 1 collagen and fibronectin, in kidneys after UUO. In contrast, these anti-fibrotic effects of CO treatment were abrogated in mice carrying null mutation of Mkk3, suggesting involvement of the MKK3 signaling pathway in mediating the CO effects. Additionally, in vitro CO exposure markedly inhibited TGF-β1-induced expression of α-SMA, collagen, and fibronectin in renal proximal tubular epithelial cells. Our findings suggest that low-dose CO exerts protective effects, via the MKK3 pathway, to inhibit development of renal fibrosis in obstructive nephropathy.

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“…In this regard, it has been shown that administration of CO can protect endothelial cells, smooth muscle cells, and neurons against apoptosis in models of ischemic injury (Dore et al, 2000;Neto et al, 2004). Conversely, blockade of HO activity can exacerbate injury in such animal models.…”

Section: Endogenous Neurotoxins and The Pathological Second Phase Of mentioning

confidence: 99%

Awareness of Hormesis Will Enhance Future Research in Basic and Applied Neuroscience

Mattson

2008

Critical Reviews in Toxicology

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Hormesis is defined operationally as responses of cells or organisms to an exogenous or intrinsic factor (chemical, temperature, psychological challenge, etc.) in which the factor induces stimulatory or beneficial effects at low doses and inhibitory or adverse effects at high doses. The compendium of articles by Calabrese entitled "Neuroscience and Hormesis" provides a broad range of examples of neurobiological processes and responses to environmental factors that exhibit biphasic dose responses, the signature of hormesis. Nerve cell networks are the "first responders" to environmental challenges-they perceive the challenge and orchestrate coordinated adaptive responses that typically involve autonomic, neuroendocrine, and behavioral changes. In addition to direct adaptive responses of neurons to environmental stressors, cells subjected to a stressor produce and release molecules such as growth factors, cytokines, and hormones that alert adjacent and even distant cells to impending danger. The discoveries that some molecules (e.g., carbon monoxide and nitric oxide) and elements (e.g., selenium and iron) that are toxic at high doses play fundamental roles in cellular signaling or metabolism suggest that during evolution, organisms (and their nervous systems) coopted environmental toxins and used them to their advantage. Neurons also respond adaptively to everyday stressors, including physical exercise, cognitive challenges, and dietary energy restriction, each of which activates pathways linked to the production of neurotrophic factors and cellular stress resistance proteins. The development of interventions that activate hormetic signaling pathways in neurons is a promising new approach for the preventation and treatment of a range of neurological disorders. COMMENTARY ON NEUROSCIENCE AND HORMESISThe biphasic nature of responses to neurotransmitters, neurotrophic factors, cytokines, drugs of abuse, and treatments for a range of neurological disorders is underappreciated and often ignored in basic and applied neuroscience research. Calabrese demonstrates a broad understanding of basic principles of neuroscience, to which he applies his expertise in toxicology and hormesis to catalog hundreds of examples of "toxins," pharmacological agents, intrinsic signaling molecules, and behavioral factors that exhibit biphasic dose responses. The focus throughout the series of articles in "Neuroscience and Hormesis" is on the results of cell culture and in vivo experiments in which the effects of increasing doses of exogenous agents (toxins, neurotransmitters, peptide, hormones, drugs of abuse, etc.) on neuronal survival or plasticity or on animal behavior has been investigated. Calabrese aptly explores the existence of hormesis in most of the major areas of the field of neuroscience, ranging from developmental mechanisms (cell survival and neurite outgrowth) to synaptic plasticity to behavior to

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Protection of transplant-induced renal ischemia-reperfusion injury with carbon monoxide

Cited by 174 publications

References 47 publications

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Protective effects of low-dose carbon monoxide against renal fibrosis induced by unilateral ureteral obstruction

Awareness of Hormesis Will Enhance Future Research in Basic and Applied Neuroscience

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