Carbon Monoxide Ameliorates Renal Cold Ischemia-Reperfusion Injury With an Upregulation of Vascular Endothelial Growth Factor by Activation of Hypoxia-Inducible Factor

Faleo, Gaetano; Neto, João Seda; Kohmoto, Junichi; Tomiyama, Koji; Shimizu, Hiroko; Takahashi, Toru; Wang, Yinna; Sugimoto, Ryujiro; Choi, Augustine M.K.; Stolz, Donna B.; Carrieri, G.; McCurry, Kenneth R.; Murase, Noriko; Nakao, Atsunori

doi:10.1097/tp.0b013e31817c6f63

Cited by 76 publications

(63 citation statements)

References 44 publications

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“…Nakao and colleagues also demonstrated that lowconcentration CO inhalation provided protection against cold I/R injury in a rat kidney transplantation model. 17 Similar protective results can be achieved after storage of grafts in a UW solution saturated with CO. 18,19 Sener et al 20 demonstrated that carbon monoxide releasing molecules (CORM) supplementation in UW solution has a significant impact on decreasing cellular and graft injury, and improving rat kidney graft survival through its anti-apoptotic effects. Recently, Ruan Y et al 21 reported the protective effect of CO from CORM on renal ischemia-reperfusion injury is associated with the inhibition of high-mobility group box 1 (HMGB1) translocation and release.…”

Section: Discussionsupporting

confidence: 66%

High-pressure carbon monoxide preserves rat kidney grafts from apoptosis and inflammation

Abe

Yazawa

Fujino

et al. 2017

Laboratory Investigation

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Renal ischemia-reperfusion (I/R) injury is unavoidable in kidney transplantation (KTx) and frequently influences both short-and long-term allograft survival. Carbon monoxide (CO) has attracted attention as a medical gas with anti-inflammatory and anti-apoptotic effects. We investigated a new strategy for organ preservation using ex vivo application of high-pressure CO in an experimental rat KTx model. We preserved kidney grafts using a high-pressure chamber filled with mixed gases composed of CO and O 2 . We found that cold I/R injury resulted in progressive deterioration of renal graft function in University of Wisconsin solution, whereas CO significantly improved renal function. We confirmed that CO decreased oxidative stress and mRNA expression of proinflammatory cytokines and inhibited tubular apoptosis in the early phases. Western blot analysis demonstrated that CO increased phosphatidylinositol-3 kinase and phosphorylation of Akt and p38 mitogen-activated protein kinase. Furthermore, CO significantly alleviated tubular injury scores and suppressed the development of interstitial fibrosis at 100 days after KTx. Thus, high-pressure mixed CO and O 2 gases successfully preserved rat kidney grafts for 24 h by protecting tubular epithelial cells from apoptosis and inhibiting inflammation.

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Section: Discussionsupporting

confidence: 66%

High-pressure carbon monoxide preserves rat kidney grafts from apoptosis and inflammation

Abe

Yazawa

Fujino

et al. 2017

Laboratory Investigation

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“…A protective role of IL-10 in renal IRI has been suggested in several studies, 39 -42 and a beneficial effect of VEGF on renal IRI has also been reported. 43,44 After adoptive B cell transfer into MT mice, renal expression of these cytokines was reduced to a level comparable to control mice. We also investigated the degree of fibrosis using Masson's trichrome staining on day 28 and found discordant effects of B cells on fibrosis compared with tubular atrophy.…”

Section: Discussionmentioning

confidence: 99%

B Cells Limit Repair after Ischemic Acute Kidney Injury

Jang

Gandolfo

Ko³

et al. 2010

Journal of the American Society of Nephrology

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“…In another approach from a third group as well as ours, heterozygous knockout mice for HIF-1α/ 2α (63) or knockdown mice of HIF-2α (64) were found to be more susceptible to acute ischemic injury in the kidney; and more importantly, it was reported that pharmacological activation of HIF again caused beneficial effects in terms of kidney protection (63). Activation of HIF by carbon monoxide also protected the transplanted kidney against prolonged cold ischemia in a rat model (65). These observations clearly offer new strategies to protect kidneys from ischemic injury.…”

Section: Phd Inhibitors As Therapeutic Targetsmentioning

confidence: 99%

Drug Discovery for Overcoming Chronic Kidney Disease (CKD): Prolyl-Hydroxylase Inhibitors to Activate Hypoxia-Inducible Factor (HIF) as a Novel Therapeutic Approach in CKD

Tanaka

Nangaku

2009

J Pharmacol Sci

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Abstract. Hypoxia-inducible factor (HIF) is a heterodimeric transcription factor composed of an oxygen-dependent α-subunit and constitutively expressed β subunit, which plays a central role in cellular adaptation to hypoxia by transcriptionally upregulating its target genes involved in angiogenesis, erythropoiesis, glycolysis, and so on. Recent studies demonstrated that hypoxia in the tubulointerstitium is involved in the pathology of progressive renal diseases and that HIF, which is activated in experimental kidney diseases, may serve to protect tubulointerstitium from the ischemic insult. The expression of HIF α-chains is post-translationally regulated and hydroxylation at one or two of the conserved proline residues by prolyl-hydroxylase domains (PHDs) is a critical step for the oxygen-dependent recruitment of the von Hippel-Lindau gene product (pVHL), a recognition component of the E3 ubiquitin ligase complex, and degradation of HIF-α. Conversely, modalities to inhibit the enzymatic activities of PHDs have been shown to activate HIF irrespective of oxygenation status and are regarded as candidate targets of pharmacological approaches against chronic kidney diseases characterized by hypoxia.

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Carbon Monoxide Ameliorates Renal Cold Ischemia-Reperfusion Injury With an Upregulation of Vascular Endothelial Growth Factor by Activation of Hypoxia-Inducible Factor

Abstract: These results demonstrate that the protective effect of CO against renal cold I/R injury may involve VEGF upregulation through its upstream signal, HIF-1 activation.

Cited by 76 publications

References 44 publications

High-pressure carbon monoxide preserves rat kidney grafts from apoptosis and inflammation

High-pressure carbon monoxide preserves rat kidney grafts from apoptosis and inflammation

B Cells Limit Repair after Ischemic Acute Kidney Injury

Drug Discovery for Overcoming Chronic Kidney Disease (CKD): Prolyl-Hydroxylase Inhibitors to Activate Hypoxia-Inducible Factor (HIF) as a Novel Therapeutic Approach in CKD

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