Preconditioning with soluble guanylate cyclase activation prevents postischemic inflammation and reduces nitrate tolerance in heme oxygenase-1 knockout mice

Wang, Walter; Jones, Allan W.; Wang, Meifang; Durante, William; Korthuis, Ronald J.

doi:10.1152/ajpheart.00810.2012

Cited by 20 publications

(20 citation statements)

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“…TNFα levels in the culture media were determined by ELISA using a commercially available kit (Invitrogen Corporation, Carlsbad, CA), as we previously described [36]. …”

Section: Methodsmentioning

confidence: 99%

Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide

Liu

Peyton

Durante

2017

Free Radical Biology and Medicine

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Although endothelial cells produce substantial quantities of ammonia during cell metabolism, the physiologic role of this gas in these cells is not known. In this study, we investigated if ammonia regulates the expression of heme oxygenase-1 (HO-1), and if this enzyme influences the biological actions of ammonia on endothelial cells. Exogenously administered ammonia, given as ammonium chloride or ammonium hydroxide, or endogenously generated ammonia stimulated HO-1 protein expression in cultured human and murine endothelial cells. Dietary supplementation of ammonia also induced HO-1 protein expression in murine arteries. The increase in HO-1 protein by ammonia in endothelial cells was first detected 4 hours after ammonia exposure and was associated with the induction of HO-1 mRNA, enhanced production of reactive oxygen species (ROS), and increased expression and activity of NF-E2-related factor-2 (Nrf2). Ammonia also activated the HO-1 promoter and this was blocked by mutating the antioxidant responsive element or by overexpressing dominant-negative Nrf2. The induction of HO-1 expression by ammonia was dependent on ROS formation and prevented by N-acetylcysteine or rotenone. Finally, prior treatment of endothelial cells with ammonia inhibited tumor necrosis factor-α -stimulated cell death. However, silencing HO-1 expression abrogated the protective action of ammonia and this was reversed by the administration of carbon monoxide but not bilirubin or iron. In conclusion, this study demonstrates that ammonia stimulates the expression of HO-1 in endothelial cells via the ROS-Nrf2 pathway, and that the induction of HO-1 contributes to the cytoprotective action of ammonia by generating carbon monoxide. Moreover, it identifies ammonia as a potentially important signaling gas in the vasculature that promotes endothelial cell survival.

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“…TNFα levels in the culture media were determined by ELISA using a commercially available kit (Invitrogen Corporation, Carlsbad, CA), as we previously described [36]. …”

Section: Methodsmentioning

confidence: 99%

Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide

Liu

Peyton

Durante

2017

Free Radical Biology and Medicine

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“…Definitions of leukocyte rolling, adhesion, and extravasation are described in (Turhan et al, 2004). Concentrations of BAY 41-2272 and BAY60-2770 administered in vivo were determined using drug response dosing experiments in C57BL/6 mice (Supplementary Figure 1) and based on previous studies (Wang et al, 2013;Ghosh et al, 2016). The hydroxyurea dose employed was based on previous in vivo studies from our groups (Almeida et al, 2012;Almeida et al, 2015).…”

Section: Downloaded Frommentioning

confidence: 99%

Beneficial Effects of Soluble Guanylyl Cyclase Stimulation and Activation in Sickle Cell Disease Are Amplified by Hydroxyurea: In Vitro and In Vivo Studies

Ferreira

Chweih

Lanaro

et al. 2020

J Pharmacol Exp Ther

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“…This latter effect is exacerbated by a postischemic decline in endothelial nitric oxide synthase activity and oxidation of soluble guanylyl cylase (sGC), which serves to amplify the intense inflammatory responses elicited by I/R by reducing the bioavailability of NO and ability of downstream signaling elements to respond to this antiadhesive signaling molecule [216,518]. This latter effect is exacerbated by a postischemic decline in endothelial nitric oxide synthase activity and oxidation of soluble guanylyl cylase (sGC), which serves to amplify the intense inflammatory responses elicited by I/R by reducing the bioavailability of NO and ability of downstream signaling elements to respond to this antiadhesive signaling molecule [216,518].…”

Section: Inflammation Contributes To Reperfusion Injurymentioning

confidence: 99%

“…Downstream signaling events stimulated by CGRP release include activation of BKCa channels in postcapillary venular endothelium and parenchymal cells, which may be coupled to heme oxygenase-1 (HO-1) expression during I/R 24 hrs later [515] (Figure 9). Ethanol-induced signaling may also upregulate HO-1 by an ARE/Nrf2-dependent mechanism [299], which could serve to protect soluble guanylyl cyclase from redox inactivation in reperfused tissues [216,518]. This preserves endothelial barrier function, which is now protected from neutrophil-dependent injury mechanisms during I/R.…”

Section: Ethanol Consumption and Ischemic Diseasementioning

confidence: 99%

“…Moreover, once tachyphylaxis to adenosine or NO preconditioning occurs, ischemic pre-or postconditioning are no longer effective in eliciting a protected phenotype [131,181,493]. With regard to nitrate tolerance that develops in response to repetitive NO donor preconditioning, recent work suggests soluble guanylyl cyclase may become oxidized on repeated activation by nitrates, rendering it susceptible to degradation and insensitive to NO [162,216,518]. The latter results are consistent with the concept that the cross tolerance to preconditioning induced by short bouts of ischemia or adenosine-A1-receptor agonists occurs via a mechanism involving downregulation or desensitization of adenosine A1 receptors.…”

Section: The Problem Of Tachyphylaxis To Repeated Bouts Of Preconditimentioning

confidence: 99%

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Cell Survival Programs and Ischemia /Reperfusion: Hormesis, Preconditioning, and Cardioprotection

Krenz¹,

Baines²,

Kalogeris³

et al. 2013

Colloquium Series on Integrated Systems Physiology: From Molecule to Function

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ii This e-book is an original work commissioned for the Colloquium Digital Library of Life Sciences, a curated collection of time-saving pedagogical resources for researchers and students who want to quickly get up to speed in a new area of life science/biomedical research. Each e-book available in Colloquium is an in-depth overview of a fast-moving or fundamental area of research, authored by a prominent contributor to the field. We call these resources 'Lectures' because authors are asked to provide an authoritative, state-of-the-art overview of their area of expertise, in a manner that is accessible to a broad, diverse audience of scientists (similar to a plenary or keynote lecture at a symposium/meeting/colloquium). Readers are invited to keep current with advances in various disciplines, gain insight into fields other than their own, and refresh their understanding of core concepts in cell & molecular biology. Physiology is a scientific discipline devoted to understanding the functions of the body. It addresses function at multiple levels, including molecular, cellular, organ, and system. An appreciation of the processes that occur at each level is necessary to understand function in health and the dysfunction associated with disease. Homeostasis and integration are fundamental principles of physiology that account for the relative constancy of organ processes and bodily function even in the face of substantial environmental changes. This constancy results from integrative, cooperative interactions of chemical and electrical signaling processes within and between cells, organs and systems. This eBook series on the broad field of physiology covers the major organ systems from an integrative perspective that addresses the molecular and cellular processes that contribute to homeostasis. Material on pathophysiology is also included throughout the eBooks. The state-of the-art treatises were produced by leading experts in the field of physiology. Each eBook includes stand-alone information and is intended to be of value to students, scientists, and clinicians in the biomedical sciences. Since physiological concepts are an ever-changing work-in-progress, each contributor will have the opportunity to make periodic updates of the covered material.Published titles (for future titles please see the website, www.morganclaypool.com/page/lifesci) ABSTRACTThe major purpose of this book is to review the evidence supporting the concept that intrinsic cell survival programs can be activated by a variety of mildly noxious stimuli or pharmacologic agents to confer protection against the deleterious effects of ischemia/reperfusion (I/R). We begin with a discussion of the concept of hormesis (a term used most extensively in the toxicologic literature which refers to biphasic cellular responses that depend on concentration or intensity of a stimulus), review the seminal studies that led to the discovery of the cardioprotective effects of ischemic preconditioning, and outline its therapeutic potential (Chapter 1). This is followed ...

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Preconditioning with soluble guanylate cyclase activation prevents postischemic inflammation and reduces nitrate tolerance in heme oxygenase-1 knockout mice

Abstract: Wang WZ, Jones AW, Wang M, Durante W, Korthuis RJ. Preconditioning with soluble guanylate cyclase activation prevents postischemic inflammation and reduces nitrate tolerance in heme oxygenase-1 knockout mice.

Cited by 20 publications

References 49 publications

Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide

Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide

Beneficial Effects of Soluble Guanylyl Cyclase Stimulation and Activation in Sickle Cell Disease Are Amplified by Hydroxyurea: In Vitro and In Vivo Studies

Cell Survival Programs and Ischemia /Reperfusion: Hormesis, Preconditioning, and Cardioprotection

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