Polyubiquitination of p62/SQSTM1 is a prerequisite for Fas/CD95 aggregation to promote caspase-dependent apoptosis in cadmium-exposed mouse monocyte RAW264.7 cells

Jung, Ki Tae; Oh, Seon-Hee

doi:10.1038/s41598-019-48684-2

Cited by 12 publications

(9 citation statements)

References 51 publications

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“…Therefore, these observations indicate that the induction of autophagy that is triggered by SRV-8 infection plays an important role in recruiting procaspase-8 to the expanding autophagosomal membrane to initiate caspase-8/-3 cascade in the Jurkat cells, which are in line with previous reports showing that the autophagosomal membrane serves as a platform for the formation of iDISC to mediate the activation of caspase-8 [30,32,[67][68][69]. So far, several autophagic proteins have been proposed as the components of iDISC, including LC3, p62/SQSTM1, and ATG5 [32,68,70,71]. We also noticed that the interaction between LC3 and procaspase-8 was enhanced during SRV-8 infection of Jurkat cells.…”

Section: Discussionsupporting

confidence: 87%

Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes

Zhu

Yang

Zhang

et al. 2020

Viruses

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Autophagy and apoptosis are two important evolutionarily conserved host defense mechanisms against viral invasion and pathogenesis. However, the association between the two pathways during the viral infection of T lymphocytes remains to be elucidated. Simian type D retrovirus (SRV) is an etiological agent of fatal simian acquired immunodeficiency syndrome (SAIDS), which can display disease features that are similar to acquired immunodeficiency syndrome in humans. In this study, we demonstrate that infection with SRV-8, a newly isolated subtype of SRV, triggered both autophagic and apoptotic pathways in Jurkat T lymphocytes. Following infection with SRV-8, the autophagic proteins LC3 and p62/SQSTM1 interacted with procaspase-8, which might be responsible for the activation of the caspase-8/-3 cascade and apoptosis in SRV-8-infected Jurkat cells. Our findings indicate that autophagic responses to SRV infection of T lymphocytes promote the apoptosis of T lymphocytes, which, in turn, might be a potential pathogenetic mechanism for the loss of T lymphocytes during SRV infection.

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Section: Discussionsupporting

confidence: 87%

Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes

Zhu

Yang

Zhang

et al. 2020

Viruses

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“…In the process of autophagy, the conversion of LC3-I (free form) to LC3-II (phosphatidylethanolamine-conjugated form) represents a key step in autophagosome formation in mammals ( Chen et al, 2010 ). p62/SQSTM1 is a selective autophagy adaptor that shuttles ubiquitinated proteins to autophagosomes or proteasomes by recognizing LC3-II ( He et al, 2018 ; Jung and Oh, 2019 ). In our previous study, we have reported impaired autophagy flux in a similar rotenone complex I inhibition cellular PD model.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-Like Peptide-1 Receptor Agonist Ameliorates 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) Neurotoxicity Through Enhancing Mitophagy Flux and Reducing α-Synuclein and Oxidative Stress

Lin

et al. 2021

Front. Mol. Neurosci.

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Parkinson disease (PD) is the second most common neurodegenerative disease without known disease modification therapy to slow down disease progression. This disease has pathological features of Lewy bodies with α-synuclein aggregation being the major component and selective dopaminergic neuronal loss over the substantia nigra. Although the exact etiology is still unknown, mitochondrial dysfunction has been shown to be central in PD pathophysiology. Type 2 diabetes mellitus has recently been connected to PD, and anti-diabetic drugs, such as glucagon-like peptide-1 receptor agonists (GLP-1RAs), have been shown to possess neuroprotective effects in PD animal models. The GLP-1RA liraglutide is currently under a phase 2 clinical trial to measure its effect on motor and non-motor symptoms in PD patients. In this study, we used an acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD to test the possible mechanism of the GLP-1RA liraglutide in the pathogenesis of PD. We show that the neurobehavioral and motor dysfunction caused by the mitochondrial complex I inhibitor, MPTP, can be partially reversed by liraglutide. The GLP-1RA can protect mice from apoptosis of substantia nigra neurons induced by MPTP. MPTP treatment led to imbalanced mitochondrial fusion and fission dynamics, altered mitochondrial morphology, impeded autophagy flux, increased α-synuclein accumulation, and elevated oxidative stress. Specifically, the normalizing of mitochondrial fusion-fission dynamic-related proteins and enhancement of autophagy flux after administration of liraglutide is associated with improving neuronal survival. This suggests that GLP-1RAs may provide potential beneficial effects for PD caused by mitochondrial dysfunction through improvement of mitochondrial morphology balance and enhancing damaged organelle degradation.

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“…Mutations in Sequestosome-1 (SQSTM1) was initially discovered in patients with Paget's disease of bone (Laurin et al, 2002) and linked to ALS and behavioral FTD in 2011 (Fecto et al, 2011). SQSTM1 encodes p62, a multifunctional protein involved in a wide range of cellular functions, including apoptosis (Jung and Oh, 2019), NFKB1 signaling (Foster et al, 2019), ubiquitinmediated autophagy (Zaffagnini et al, 2018;Gao et al, 2019;Park et al, 2019), and transcription regulation (Rea et al, 2013). p62 is also a standard component of ubiquitin-containing inclusions in several neurological disorders, including ALS and FTD.…”

Section: Sequestosome-1 (Sqstm1)mentioning

confidence: 99%

The Overlapping Genetics of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

et al. 2020

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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two diseases that form a broad neurodegenerative continuum. Considerable effort has been made to unravel the genetics of these disorders, and, based on this work, it is now clear that ALS and FTD have a significant genetic overlap. TARDBP, SQSTM1, VCP, FUS, TBK1, CHCHD10, and most importantly C9orf72, are the critical genetic players in these neurological disorders. Discoveries of these genes have implicated autophagy, RNA regulation, and vesicle and inclusion formation as the central pathways involved in neurodegeneration. Here we provide a summary of the significant genes identified in these two intrinsically linked neurodegenerative diseases and highlight the genetic and pathological overlaps.

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Polyubiquitination of p62/SQSTM1 is a prerequisite for Fas/CD95 aggregation to promote caspase-dependent apoptosis in cadmium-exposed mouse monocyte RAW264.7 cells

Cited by 12 publications

References 51 publications

Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes

Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes

Glucagon-Like Peptide-1 Receptor Agonist Ameliorates 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) Neurotoxicity Through Enhancing Mitophagy Flux and Reducing α-Synuclein and Oxidative Stress

The Overlapping Genetics of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

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