The peroxynitrite donor 3-morpholinosydnonimine activates Nrf2 and the UPR leading to a cytoprotective response in endothelial cells

Mattart, Laurine; Calay, Damien; Simon, Dorothy; Roebroeck, Laura; Caesens-Koenig, Ludmilla; Steenbrugge, Martine Van; Tevel, Virginie; Michiels, Carine; Arnould, Thierry; Boudjeltia, Karim Zouaoui; Raes, Martine

doi:10.1016/j.cellsig.2011.09.002

Cited by 23 publications

(19 citation statements)

References 51 publications

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“…Bcl-2 family proteins also regulate autophagy, a type of cell death, occurring under both basal conditions and conditions of stress (i.e. starvation), which represents a cellular defensive mechanism able to eliminate also ROS induced damaged proteins [35,36].…”

Section: Discussionmentioning

confidence: 99%

Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression

Mollace

Gliozzi

Musolino

et al. 2015

International Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression

Mollace

Gliozzi

Musolino

et al. 2015

International Journal of Cardiology

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“…23 Moreover, several natural compounds with anti-inflammatory or antioxidant activity (eg, curcumin, vitamin D, resveratrol, or the analogue pterostilbene) [24][25][26][27][28] promote autophagy in ECs to protect against endothelial inflammation or oxidative stress. However, oxidative stress induced by ROS or oxLDL may also affect the endoplasmic reticulum (ER), 20,29 inducing deregulation of cytosolic calcium, a condition known to trigger ER stress and apoptosis. Splicing of the mRNA of X-box-binding protein 1, which is an important event during ER stress, allows formation of a potent transcription factor in ECs that triggers an autophagic response through transcriptional activation of the autophagy regulator Beclin 1.…”

Section: Autophagy In the Normal Vessel Wall Autophagy Is A Cytoprotementioning

confidence: 99%

“…Autophagy in vascular endothelial cells (ECs) is a protective mechanism against many pathophysiological stimuli, including oxidized low-density lipoprotein (oxLDL), 19 reactive oxygen species (ROS), 20 lipopolysaccharides, 21 hypoxia, 22 and advanced glycation end products. 23 Moreover, several natural compounds with anti-inflammatory or antioxidant activity (eg, curcumin, vitamin D, resveratrol, or the analogue pterostilbene) [24][25][26][27][28] promote autophagy in ECs to protect against endothelial inflammation or oxidative stress.…”

Section: Autophagy In the Normal Vessel Wall Autophagy Is A Cytoprotementioning

confidence: 99%

Autophagy in Vascular Disease

Meyer

Grootaert

Michiels

et al. 2015

Circulation Research

254

179

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A utophagy is a complex intracellular process that delivers cytoplasmic constituents for degradation into lysosomes.1,2 Three main types of autophagy have been described: (1) microautophagy, comprising direct engulfment of cytoplasmic material by lysosomes via inward invaginations of the lysosomal membrane, (2) macroautophagy, characterized by formation of double-membrane sequestering compartments termed autophagosomes that fuse with lysosomes for delivery of cytoplasmic cargo, and (3) chaperone-mediated autophagy, mediated by a chaperone complex and lysosomal-associated membrane protein type 2A to degrade cytosolic proteins with a specific targeting motif. The term autophagy usually refers to macroautophagy, which is the most prevalent and beststudied form of autophagy. Also in this review, we will focus exclusively on macroautophagy, further cited as autophagy.Autophagy occurs at basal levels in most tissues to allow constitutive turnover of cytosolic components but is stimulated by environmental stress-related signals (eg, nutrient deprivation and oxidative injury) to recycle nutrients and to generate energy for maintenance of cell viability in unfavorable conditions.1 In addition to cellular stress, basal autophagy can be intensified by specific drugs, 3 indicating that the autophagic machinery is a potential therapeutic target for diverse diseases. Indeed, given that autophagy is involved in the prevention

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“…Nrf2 appears to be involved in the regulation of protein aggregation in autophagic substrate selection (43) as well as autophagy per se (44)(45)(46)(47). Although it remains unclear whether the observed increased steady state levels of autophagosomes in Nrf2-deficient breast cancer cells, endothelial cells, and airway epithelial cells are caused by an impairment of autophagosome clearance (44,46,47), it has been demonstrated that Nrf2 is a critical mediator of autophagic clearance of ubiquitinated protein aggregates in macrophages (45).…”

Section: Nrf2 In Autophagymentioning

confidence: 99%

“…Although it remains unclear whether the observed increased steady state levels of autophagosomes in Nrf2-deficient breast cancer cells, endothelial cells, and airway epithelial cells are caused by an impairment of autophagosome clearance (44,46,47), it has been demonstrated that Nrf2 is a critical mediator of autophagic clearance of ubiquitinated protein aggregates in macrophages (45). In addition, a recent study showed that Nrf2 is capable of clearing phosphorylated tau by induction of nuclear dot protein 52 (NDP52), an autophagy adaptor protein (also known as CALCOCO2) in the presence of autophagy stimulator thereby potentially contributing to brain protection (48).…”

Section: Nrf2 In Autophagymentioning

confidence: 99%

Nuclear factor erythroid-2 related factor 2 Nrf2 -mediated protein quality control in cardiomyocytes

et al. 2016

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Protein quality control (PQC) acts to minimize the level and toxicity of malfolded proteins in the cell. It is performed by an elaborate network of molecular chaperones and targeted protein degradation pathways. PQC monitors and maintains protein homeostasis or proteostasis in the cells. Whilst chaperones may actively promote refolding of malfolded proteins, the malfolded proteins which cannot be correctly refolded are degraded by the ubiquitin proteasome system (UPS) and the autophagic-lysosome pathway (ALP). The UPS degrades individual misfolded protein molecules, whereas the ALP removes large and less soluble protein aggregates and organelles. Emerging evidence indicates that dysregulated and inadequate PQC play an important role in the pathogenesis of not only classic conformational disease but more common forms of cardiac pathology such as cardiac pathological hypertrophy and heart failure. Nuclear factor erythroid 2-related factor 2 (Nrf2), a master transcription factor of cellular defense, appears to regulate the USP and the ALP by directly controlling the expression of UPS-and ALP-related genes. This article highlights an emerging role of Nrf2 in the regulation of intracellular PQC as well as its potential involvement in cardiac pathology.

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The peroxynitrite donor 3-morpholinosydnonimine activates Nrf2 and the UPR leading to a cytoprotective response in endothelial cells

Cited by 23 publications

References 51 publications

Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression

Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression

Autophagy in Vascular Disease

Nuclear factor erythroid-2 related factor 2 Nrf2 -mediated protein quality control in cardiomyocytes

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