RIP3 S-nitrosylation contributes to cerebral ischemic neuronal injury

Miao, Wanying; Qu, Zhongwei; Shi, Kejie; Zhang, Dengyue; Zong, Yan-Yan; Zhang, Gongliang; Zhang, Guangyi; Hu, Shuqun

doi:10.1016/j.brainres.2015.08.020

Cited by 17 publications

(9 citation statements)

References 28 publications

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“…This study also established that I/R-induced, RIP3-dependent, CaMKII activation to induce necroptosis occurred by a ROS-dependent mechanism involving oxidation of CaMKII at Met281 and Met282 (221). Cerebral I/R also involves RIP3 activation by a mechanism that involves NMDA receptor-mediated calcium influx to activate nNOS (562). Consequent NO production results in RIP3 S-nitrosylation at Cys119 to facilitate its activation to promote necroptosis of cerebral neurons after I/R.…”

Section: Mechanisms Underlying I/r Cell Injury and Deathmentioning

confidence: 99%

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Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

615

565

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Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease.

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Section: Mechanisms Underlying I/r Cell Injury and Deathmentioning

confidence: 99%

“…CaMK also acts to enable Ca 2+ release from cardiac SR (835), thereby contributing to calcium overload in myocardial I/R. In contrast, RIP kinases induce ROS production (562, 567) and increase intracellular levels of the death-inducing lipid, ceramide (781). …”

Section: Mechanisms Underlying I/r Cell Injury and Deathmentioning

confidence: 99%

Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

615

565

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“…Although NO has been extensively studied in relation to apoptosis, very little is known about its role in necroptosis. One study provided evidence that nitrosylation of RIPK3 is involved in ischemic neuronal injury by activating necroptosis [89]. The observations suggest that ischemia provokes NO synthase-dependent nitrosylation of RIPK3 in a manner that promotes its phosphorylation and activity [89].…”

Section: Ripk1/3mentioning

confidence: 99%

“…One study provided evidence that nitrosylation of RIPK3 is involved in ischemic neuronal injury by activating necroptosis [89]. The observations suggest that ischemia provokes NO synthase-dependent nitrosylation of RIPK3 in a manner that promotes its phosphorylation and activity [89]. However, the molecular link between elevated RIPK3 nitrosylation and phosphorylation remains to be identified.…”

Section: Ripk1/3mentioning

confidence: 99%

Oxidants, Antioxidants and Thiol Redox Switches in the Control of Regulated Cell Death Pathways

Benhar

2020

Antioxidants

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It is well appreciated that biological reactive oxygen and nitrogen species such as hydrogen peroxide, superoxide and nitric oxide, as well as endogenous antioxidant systems, are important modulators of cell survival and death in diverse organisms and cell types. In addition, oxidative stress, nitrosative stress and dysregulated cell death are implicated in a wide variety of pathological conditions, including cancer, cardiovascular and neurological diseases. Therefore, much effort is devoted to elucidate the molecular mechanisms linking oxidant/antioxidant systems and cell death pathways. This review is focused on thiol redox modifications as a major mechanism by which oxidants and antioxidants influence specific regulated cell death pathways in mammalian cells. Growing evidence indicates that redox modifications of cysteine residues in proteins are involved in the regulation of multiple cell death modalities, including apoptosis, necroptosis and pyroptosis. In addition, recent research suggests that thiol redox switches play a role in the crosstalk between apoptotic and necrotic forms of regulated cell death. Thus, thiol-based redox circuits provide an additional layer of control that determines when and how cells die.

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“…In addition to phosphorylation modification, Miao et al tested RIP3 S-nitrosylation in I/R paralleled with elevated phosphorylation. It means that phosphorylation and activation of RIP3 could be modulated by its S-nitrosylation triggered by NMDAR-dependent nNOS activation [ 37 ].…”

Section: Necroptosis In Cerebral Ischemia Diseasementioning

confidence: 99%

The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease

Zhang

et al. 2018

Behavioural Neurology

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Necroptosis is the best-described form of regulated necrosis at present, which is widely recognized as a component of caspase-independent cell death mediated by the concerted action of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Mixed-lineage kinase domain-like (MLKL) was phosphorylated by RIPK3 at the threonine 357 and serine 358 residues and then formed tetramers and translocated onto the plasma membrane, which destabilizes plasma membrane integrity leading to cell swelling and membrane rupture. Necroptosis is downstream of the tumor necrosis factor (TNF) receptor family, and also interaction with NOD-like receptor pyrin 3 (NLRP3) induced inflammasome activation. Multiple inhibitors of RIPK1 and MLKL have been developed to block the cascade of signal pathways for procedural necrosis and represent potential leads for drug development. In this review, we highlight recent progress in the study of roles for necroptosis in cerebral ischemic disease and discuss how these modifications delicately control necroptosis.

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RIP3 S-nitrosylation contributes to cerebral ischemic neuronal injury

Cited by 17 publications

References 28 publications

Ischemia/Reperfusion

Ischemia/Reperfusion

Oxidants, Antioxidants and Thiol Redox Switches in the Control of Regulated Cell Death Pathways

The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease

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