The role of DJ-1 in the oxidative stress cell death cascade after stroke

Pantcheva, Paolina; Elías, Maya N.; Duncan, Kelsey; Borlongan, Cesar V.; Tajiri, Naoki; Kaneko, Yuji

doi:10.4103/1673-5374.139458

Cited by 27 publications

(11 citation statements)

References 42 publications

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“…Mitochondrial dysfunction is monitored by several proteins, such as NIX, BNIP3, PINK1, parkin, SQSTM1 (p62) [ 31 , 78 , 79 ]. Recent work reveals that DJ-1 (PARK7) acts as a signaling hub through its ability to recognize oxidative damaged in mitochondria and induce mitophagy, thus eliminating damaged mitochondria in mammalian cells [ 39 , 80 – 82 ]. The role of DJ-1 in the regulation of oxidative stress has been extensively studied in neurodegenerative diseases [ 82 – 84 ].…”

Section: Discussionmentioning

confidence: 99%

Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

et al. 2016

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The intestinal epithelial cells contain a large number of mitochondria for persisting absorption and barrier function. Selective autophagy of mitochondria (mitophagy) plays an important role in the quality control of mitochondria and maintenance of cell homeostasis. Transmissible gastroenteritis virus (TGEV) is a porcine enteropathogenic coronavirus which induces malabsorption and lethal watery diarrhea in suckling piglets. The role of mitophagy in the pathological changes caused by TGEV infection is unclear. Here, we report that TGEV induces mitophagy to suppress oxidative stress and apoptosis induced by viral infection in porcine epithelial cells (IPEC-J2). We observe that TGEV infection induce mitochondrial injury, abnormal morphology, complete mitophagy, and without obvious apoptosis after TGEV infection. Meanwhile, TGEV also induces DJ-1 and some antioxidant genes upregulation to suppress oxidative stress induced by viral infection. Furthermore, silencing DJ-1 inhibit mitophagy and increase apoptosis after TGEV infection. In addition, we demonstrate for the first time that viral nucleocapsid protein (N) is located in mitochondria and mitophagosome during virus infection or be expressed alone. Those results provide a novel perspective for further improvement of prevention and treatment in TGEV infection. These results suggest that TGEV infection induce mitophagy to promote cell survival and possibly viral infection.

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Section: Discussionmentioning

confidence: 99%

Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

et al. 2016

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“…Parkinson's disease-associated proteins in mitochondrial homeostasis DJ-1: a short ubiquitous protein with chaperone activity. Protects cells from oxidative stress and mitochondrial injury ( Blackinton et al, 2009 ; Pantcheva et al, 2014 ). DJ-1 partners with PINK1 and Parkin to regulate mitochondrial homeostasis ( Xiong et al, 2009 ).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dynamics in Parkinson's disease: a role for α-synuclein?

Devoto

Falzone

2017

Disease Models &Amp; Mechanisms

142

131

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The distinctive pathological hallmarks of Parkinson's disease are the progressive death of dopaminergic neurons and the intracellular accumulation of Lewy bodies enriched in α-synuclein protein. Several lines of evidence from the study of sporadic, familial and pharmacologically induced forms of human Parkinson's disease also suggest that mitochondrial dysfunction plays an important role in disease progression. Although many functions have been proposed for α-synuclein, emerging data from human and animal models of Parkinson's disease highlight a role for α-synuclein in the control of neuronal mitochondrial dynamics. Here, we review the α-synuclein structural, biophysical and biochemical properties that influence relevant mitochondrial dynamic processes such as fusion-fission, transport and clearance. Drawing on current evidence, we propose that α-synuclein contributes to the mitochondrial defects that are associated with the pathology of this common and progressive neurodegenerative disease.

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“…Oxidative stress is a well-known common hallmark closely implicated in the progression of lifestyle-related diseases, including obesity, ischemic disease, atherosclerosis, and arthritis [ 6 ]. There is emerging evidence that reactive oxygen species (ROS) are generated in various mammalian cells upon interaction with environmental stress and play roles as signaling molecules in neuronal cells [ 7 – 9 ].…”

Section: Introductionmentioning

confidence: 99%

Phlorofucofuroeckol Improves Glutamate-Induced Neurotoxicity through Modulation of Oxidative Stress-Mediated Mitochondrial Dysfunction in PC12 Cells

et al. 2016

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Stroke is a complex neurodegenerative disorder with a clinically high prevalence and mortality. Despite many efforts to protect against ischemic stroke, its incidence and related permanent disabilities continue to increase. In this study, we found that pretreatment with phlorofucofuroeckol (PFF), isolated from brown algae species, significantly increased cell viability in glutamate-stimulated PC12 cells. Additionally, glutamate-stimulated cells showed irregular morphology, but PFF pretreatment resulted in improved cell morphology, which resembled that in cells cultured under normal conditions. We further showed that PFF pretreatment effectively inhibited glutamate-induced apoptotic cell death in a caspase-dependent manner. Reactive oxygen species (ROS) induced by oxidative stress are closely associated with ischemia-induced neurological diseases. Exposure of PC12 cells to glutamate induced abundant production of intracellular ROS and mitochondrial dysfunction, which was attenuated by PFF in a dose-dependent manner. In vivo studies revealed that PFF-mediated prevention was achieved predominantly through inhibition of apoptosis and mitochondrial ROS generation. Taken together, these results suggest the possibility of PFF as a neuroprotective agent in ischemic stroke.

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The role of DJ-1 in the oxidative stress cell death cascade after stroke

Cited by 27 publications

References 42 publications

Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

Mitophagy in TGEV infection counteracts oxidative stress and apoptosis

Mitochondrial dynamics in Parkinson's disease: a role for α-synuclein?

Phlorofucofuroeckol Improves Glutamate-Induced Neurotoxicity through Modulation of Oxidative Stress-Mediated Mitochondrial Dysfunction in PC12 Cells

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