COVID-19 and Parkinson’s Disease: Shared Inflammatory Pathways Under Oxidative Stress
The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson’s disease (PD). Increasing evidence suggests an involvemen...
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| Published in | Brain Sciences Vol. 10; no. 11; p. 807 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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31.10.2020
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| ISSN | 2076-3425 2076-3425 |
| DOI | 10.3390/brainsci10110807 |
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| Abstract | The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson’s disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NFκB in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NFκB-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson’s like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NFκB pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NFκB and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NFκB activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD. |
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| AbstractList | The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson’s disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NFκB in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NFκB-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson’s like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NFκB pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NFκB and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NFκB activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD. The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson's disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NF[kappa]B in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NF[kappa]B-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson's like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NF[kappa]B pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NF[kappa]B and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NF[kappa]B activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD. The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson's disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NF[kappa]B in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NF[kappa]B-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson's like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NF[kappa]B pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NF[kappa]B and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NF[kappa]B activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD. Keywords: Parkinson's disease; SARS-CoV-2; caspase; inhibitors; nuclear factor kappa B (NF[kappa]B); 6OHDA; oxidative stress; apoptosis The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson's disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NFκB in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NFκB-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson's like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NFκB pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NFκB and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NFκB activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD.The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson's disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NFκB in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NFκB-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson's like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NFκB pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NFκB and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NFκB activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD. |
| Audience | Academic |
| Author | Ahmad, Bushra Y Janjua, Najma Cami-Kobeci, Gerta Klenja, Donika Chaudhry, Zaharah L |
| AuthorAffiliation | 1 Institute of Biomedical & Environmental Science and Technology, School of Life Sciences, Faculty of Creative Arts, Technologies & Science, University Square, University of Bedfordshire, Luton LU1 3JU, UK; zohara.chaudhry@beds.ac.uk (Z.L.C.); Gerta.Cami-Kobeci@beds.ac.uk (G.C.-K.) 3 Faculty of Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan; jann@med.kawasaki-m.ac.jp 2 School of Cellular and Molecular Medicine, University of Bristol, University Walk, Bristol BS8 1TD, UK; wo18459@bristol.ac.uk |
| AuthorAffiliation_xml | – name: 1 Institute of Biomedical & Environmental Science and Technology, School of Life Sciences, Faculty of Creative Arts, Technologies & Science, University Square, University of Bedfordshire, Luton LU1 3JU, UK; zohara.chaudhry@beds.ac.uk (Z.L.C.); Gerta.Cami-Kobeci@beds.ac.uk (G.C.-K.) – name: 3 Faculty of Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan; jann@med.kawasaki-m.ac.jp – name: 2 School of Cellular and Molecular Medicine, University of Bristol, University Walk, Bristol BS8 1TD, UK; wo18459@bristol.ac.uk |
| Author_xml | – sequence: 1 fullname: Chaudhry, Zaharah L – sequence: 2 fullname: Klenja, Donika – sequence: 3 fullname: Janjua, Najma – sequence: 4 fullname: Cami-Kobeci, Gerta – sequence: 5 fullname: Ahmad, Bushra Y |
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| Cites_doi | 10.1002/bies.1089 10.1016/j.brainres.2011.02.092 10.1186/s12974-018-1193-6 10.1042/BJ20052026 10.3233/JPD-160804 10.4172/2161-0460.1000461 10.12659/MSMBR.910307 10.1016/S0006-291X(03)00309-7 10.1523/JNEUROSCI.5175-08.2009 10.1186/s12576-020-00743-4 10.1128/MCB.01430-12 10.1016/S0140-6736(20)30251-8 10.1074/jbc.M203885200 10.1016/j.thromres.2019.07.013 10.18632/aging.103511 10.1016/j.tiv.2005.01.006 10.1038/366580a0 10.1016/j.cell.2020.02.052 10.5607/en.2015.24.4.325 10.1038/sj.cdd.4402047 10.1038/s41423-020-0485-9 10.1016/j.bbabio.2009.03.010 10.1016/j.abb.2019.05.011 10.1002/emmm.201000080 10.1016/j.resp.2011.09.012 10.1016/j.tcb.2012.08.001 10.1038/sj.onc.1205255 10.1212/WNL.0b013e3182703f76 10.1073/pnas.94.14.7531 10.1152/japplphysiol.00391.2007 10.1016/j.dsx.2020.04.020 10.1038/nrmicro.2016.81 10.1074/jbc.M307774200 10.1073/pnas.0704908104 10.1152/ajprenal.00166.2017 10.1016/j.bbadis.2009.09.002 10.1016/j.immuni.2020.04.003 10.1038/sj.embor.7400380 10.1016/j.redox.2017.02.014 10.1146/annurev.biochem.74.082803.133400 10.1016/S0006-2952(99)00296-8 10.1016/j.freeradbiomed.2014.03.011 10.1016/j.freeradbiomed.2009.10.045 10.1016/S0301-0082(01)00003-X 10.1046/j.1471-4159.2000.0741384.x 10.1016/j.cytogfr.2020.05.002 10.1016/j.nbd.2013.08.007 10.1038/ni.3279 10.1006/exnr.2002.7891 10.5607/en.2015.24.2.103 10.1097/WNR.0b013e328364d616 10.1016/j.neulet.2013.08.020 10.1124/mol.63.4.784 10.3390/v12060646 10.1016/j.redox.2015.08.016 10.1152/ajpregu.00057.2009 10.3389/fnana.2015.00091 10.1038/s41586-020-2012-7 10.1016/S0140-6736(20)30183-5 10.4062/biomolther.2018.047 10.1523/JNEUROSCI.5537-06.2007 10.3349/ymj.2015.56.3.862 10.1101/cshperspect.a009365 10.1016/j.freeradbiomed.2006.10.047 10.1038/ncomms12849 |
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| References | Chen (ref_9) 2018; 15 Hunot (ref_45) 1997; 94 Erekat (ref_46) 2018; 24 ref_12 ref_55 Nicholls (ref_28) 2009; 1787 Midwinter (ref_18) 2006; 396 Kim (ref_65) 2013; 60 Kim (ref_66) 2002; 277 Han (ref_52) 2019; 27 Apelbaum (ref_61) 2013; 33 Gazewood (ref_26) 2013; 87 Tornatore (ref_16) 2012; 22 Chaudhry (ref_44) 2014; 4 Hyrc (ref_74) 2003; 63 McStay (ref_53) 2014; 2014 Bowie (ref_15) 2000; 59 Henn (ref_48) 2007; 27 Ho (ref_73) 2009; 29 Huang (ref_2) 2020; 395 Gupta (ref_20) 2019; 181 Shuai (ref_67) 1993; 366 Lalley (ref_35) 2009; 296 ref_68 Nile (ref_6) 2020; 53 Dong (ref_21) 2020; 12 Glinka (ref_34) 1995; 292 Blesa (ref_40) 2015; 9 Lu (ref_3) 2020; 395 Lamkanfi (ref_72) 2007; 14 Zhang (ref_59) 2015; 16 Jia (ref_14) 2007; 42 Falzarano (ref_1) 2016; 14 Jiang (ref_69) 2012; 79 Deumens (ref_30) 2002; 175 Cha (ref_13) 2015; 56 Cookson (ref_51) 2005; 74 Astuti (ref_57) 2020; 14 Asanuma (ref_75) 2004; 58 Moon (ref_42) 2015; 24 Alva (ref_22) 2017; 12 Krappmann (ref_19) 2005; 6 Ramos (ref_24) 2014; 71 Sinkovics (ref_10) 2015; 47 Baille (ref_36) 2016; 16 Ghosh (ref_47) 2007; 104 Hoffmann (ref_5) 2020; 181 Zhou (ref_4) 2020; 579 Niizuma (ref_27) 2010; 1802 Tirmenstein (ref_32) 2005; 19 Benigni (ref_8) 2010; 2 Kim (ref_41) 2015; 24 Blum (ref_33) 2001; 65 Niizuma (ref_25) 2009; 109 Ye (ref_71) 2013; 553 Dimova (ref_23) 2015; 6 Kumar (ref_11) 2017; 313 Butturini (ref_64) 2019; 669 Cassarino (ref_43) 2000; 74 Donnelly (ref_31) 2007; 103 Andersen (ref_50) 2001; 23 Salvesen (ref_54) 2012; 824 Flood (ref_17) 2011; 2011 Masumoto (ref_70) 2003; 303 Gong (ref_39) 2017; 14 Xiang (ref_49) 2011; 1387 Sironi (ref_62) 2004; 279 Ahmed (ref_56) 2013; 24 Iwata (ref_58) 2016; 7 Ren (ref_63) 2020; 8 Hirano (ref_7) 2020; 52 Seccombe (ref_37) 2011; 179 Andrzejewski (ref_29) 2020; 70 Kalivendi (ref_38) 2010; 48 Fulda (ref_60) 2002; 21 |
| References_xml | – volume: 23 start-page: 640 year: 2001 ident: ref_50 article-title: Does neuronal loss in Parkinson’s disease involve programmed cell death? publication-title: Bioessays doi: 10.1002/bies.1089 – volume: 1387 start-page: 29 year: 2011 ident: ref_49 article-title: Cathepsin L is involved in 6-hydroxydopamine induced apoptosis of SH-SY5Y neuroblastoma cells publication-title: Brain Res. doi: 10.1016/j.brainres.2011.02.092 – volume: 15 start-page: 150 year: 2018 ident: ref_9 article-title: Valproic acid attenuates traumatic spinal cord injury-induced inflammation via STAT1 and NF-κB pathway dependent of HDAC3 publication-title: J. Neuroinflamm. doi: 10.1186/s12974-018-1193-6 – volume: 47 start-page: 1211 year: 2015 ident: ref_10 article-title: The cnidarian origin of the proto-oncogenes NF-κB/STAT and WNT-like oncogenic pathway drives the ctenophores publication-title: Int. J. Oncol. – volume: 824 start-page: 113 year: 2012 ident: ref_54 article-title: Proliferative versus apoptotic functions of caspase-8 Hetero or homo: The caspase-8 dimer controls cell fate publication-title: Biochimica Biophysica Acta – volume: 396 start-page: 71 year: 2006 ident: ref_18 article-title: IkappaB is a sensitive target for oxidation by cell-permeable chloramines: Inhibition of NF-kappaB activity by glycine chloramine through methionine oxidation publication-title: Biochem. J. doi: 10.1042/BJ20052026 – volume: 16 start-page: 463 year: 2016 ident: ref_36 article-title: Ventilatory dysfunction in Parkinson’s disease publication-title: J. Parkinson’s Dis. doi: 10.3233/JPD-160804 – ident: ref_55 doi: 10.4172/2161-0460.1000461 – volume: 24 start-page: 120 year: 2018 ident: ref_46 article-title: Association of Parkinson disease induction with cardiac upregulation of apoptotic mediators P53 and active caspase-3: An immunohistochemistry study publication-title: Med. Sci. Monit. Basic Res. doi: 10.12659/MSMBR.910307 – volume: 303 start-page: 69 year: 2003 ident: ref_70 article-title: ASC is an activating adaptor for NF-kappa B and caspase-8-dependent apoptosis publication-title: Biochem. Biophys. Res. Commun. doi: 10.1016/S0006-291X(03)00309-7 – volume: 29 start-page: 1011 year: 2009 ident: ref_73 article-title: The Parkinson disease protein leucine-rich repeat kinase 2 transduces death signals via fas-associated protein with death domain and caspase-8 in a cellular model of neurodegeneration publication-title: J. Neurosci. doi: 10.1523/JNEUROSCI.5175-08.2009 – volume: 70 start-page: 16 year: 2020 ident: ref_29 article-title: Respiratory pattern and phrenic and hypoglossal nerve activity during normoxia and hypoxia in 6-OHDA-induced bilateral model of Parkinson’s disease. 25 publication-title: J. Physiol. Sci. doi: 10.1186/s12576-020-00743-4 – volume: 33 start-page: 800 year: 2013 ident: ref_61 article-title: Type I interferons induce apoptosis by balancing cFLIP and caspase-8 independent of death ligands publication-title: Mol. Cell. Biol. doi: 10.1128/MCB.01430-12 – volume: 395 start-page: 565 year: 2020 ident: ref_3 article-title: Genomic characterisation and epidemiology of 2019 novel coronavirus: Implications for virus origins and receptor binding publication-title: Lancet doi: 10.1016/S0140-6736(20)30251-8 – volume: 277 start-page: 40594 year: 2002 ident: ref_66 article-title: JAK-STAT signaling mediates gangliosides-induced inflammatory responses in brain microglial cells publication-title: J. Biol. Chem. doi: 10.1074/jbc.M203885200 – volume: 181 start-page: 77 year: 2019 ident: ref_20 article-title: The stimulation of thrombosis by hypoxia publication-title: Thromb. Res. doi: 10.1016/j.thromres.2019.07.013 – volume: 12 start-page: 13791 year: 2020 ident: ref_21 article-title: Pathophysiology of SARS-CoV-2 infection in patients with intracerebral hemorrhage publication-title: Aging doi: 10.18632/aging.103511 – volume: 19 start-page: 471 year: 2005 ident: ref_32 article-title: Effects of 6-hydroxydopamine on mitochondrial function and glutathione status in SH-SY5Y human neuroblastoma cells publication-title: Toxicol. In Vitro doi: 10.1016/j.tiv.2005.01.006 – volume: 366 start-page: 580 year: 1993 ident: ref_67 article-title: Polypeptide signalling to the nucleus through tyrosine phosphorylation of Jak and Stat proteins publication-title: Nature doi: 10.1038/366580a0 – volume: 2011 start-page: 216298 year: 2011 ident: ref_17 article-title: Transcriptional factor NF-κB as a target for therapy in Parkinson’s disease publication-title: Parkinson’s Dis. – volume: 181 start-page: 271 year: 2020 ident: ref_5 article-title: SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor publication-title: Cell doi: 10.1016/j.cell.2020.02.052 – volume: 24 start-page: 325 year: 2015 ident: ref_41 article-title: The role of oxidative stress in neurodegenerative diseases publication-title: Exp. Neurobiol. doi: 10.5607/en.2015.24.4.325 – volume: 14 start-page: 44 year: 2007 ident: ref_72 article-title: Caspase in cell survival, proliferation and differentiation publication-title: Cell Death Differ. doi: 10.1038/sj.cdd.4402047 – volume: 8 start-page: 881 year: 2020 ident: ref_63 article-title: The ORF3a protein of SARS-CoV-2 induces apoptosis in cells publication-title: Cell. Mol. Immunol. doi: 10.1038/s41423-020-0485-9 – volume: 1787 start-page: 1416 year: 2009 ident: ref_28 article-title: Mitochondrial calcium function and dysfunction in the central nervous system publication-title: Biochimica Biophysica Acta doi: 10.1016/j.bbabio.2009.03.010 – volume: 669 start-page: 22 year: 2019 ident: ref_64 article-title: STAT1 drives M1 microglia activation and neuroinflammation under Hypoxia publication-title: Arch. Biochem. Biophys. doi: 10.1016/j.abb.2019.05.011 – volume: 2014 start-page: 799 year: 2014 ident: ref_53 article-title: Measuring apoptosis: Caspase inhibitors and activity assays publication-title: Cold Spring Harb. Protoc. – volume: 2 start-page: 247 year: 2010 ident: ref_8 article-title: Angiotensin II revisited: New roles in inflammation, immunology and aging publication-title: EMBO Mol. Med. doi: 10.1002/emmm.201000080 – volume: 87 start-page: 267 year: 2013 ident: ref_26 article-title: Parkinson disease: An update publication-title: Am. Fam. Physician – volume: 179 start-page: 300 year: 2011 ident: ref_37 article-title: Abnormal ventilatory control in Parkinson’s disease- further evidence for non-motor dysfunction publication-title: Respir. Physiol. Neurobiol. doi: 10.1016/j.resp.2011.09.012 – volume: 22 start-page: 557 year: 2012 ident: ref_16 article-title: The nuclear factor kappa B signaling pathway: Integrating metabolism with inflammation publication-title: Trends Cell Biol. doi: 10.1016/j.tcb.2012.08.001 – volume: 21 start-page: 2295 year: 2002 ident: ref_60 article-title: IFNγ sensitizes for apoptosis by upregulating caspase-8 expression through the Stat1 pathway publication-title: Oncogene doi: 10.1038/sj.onc.1205255 – volume: 79 start-page: 1767 year: 2012 ident: ref_69 article-title: Bid signal pathway components are identified in the temporal cortex with Parkinson disease publication-title: Neurology doi: 10.1212/WNL.0b013e3182703f76 – volume: 94 start-page: 7531 year: 1997 ident: ref_45 article-title: Nuclear translocation of NF-kappaB is increased in dopaminergic neurons of patients with Parkinson disease publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.94.14.7531 – volume: 103 start-page: 1269 year: 2007 ident: ref_31 article-title: Hypoxia transduction by carotid body chemoreceptors in mice lacking dopamine D(2) receptors publication-title: J. Appl. Physiol. doi: 10.1152/japplphysiol.00391.2007 – volume: 4 start-page: 1 year: 2014 ident: ref_44 article-title: The role of Caspase in Parkinson’s disease pathogenesis: A brief look at the mitochondrial pathway publication-title: Austin J. Alzheimer’s Parkinson’s Dis. – volume: 14 start-page: 407 year: 2020 ident: ref_57 article-title: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): An overview of viral structure and host response publication-title: Diabetes Metab. Syndr. doi: 10.1016/j.dsx.2020.04.020 – volume: 14 start-page: 523 year: 2016 ident: ref_1 article-title: SARS and MERS: Recent insights into emerging coronaviruses publication-title: Nat. Rev. Microbiol. doi: 10.1038/nrmicro.2016.81 – volume: 279 start-page: 4066 year: 2004 ident: ref_62 article-title: STAT1-induced apoptosis is mediated by caspase 2, 3, and 7 publication-title: J. Biol. Chem. doi: 10.1074/jbc.M307774200 – volume: 104 start-page: 18754 year: 2007 ident: ref_47 article-title: Selective inhibition of NF-kappaB activation prevents dopaminergic neuronal loss in a mouse model of Parkinson’s disease publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.0704908104 – volume: 109 start-page: S133 year: 2009 ident: ref_25 article-title: Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival publication-title: J. Neurosci. – volume: 313 start-page: F781 year: 2017 ident: ref_11 article-title: Inhibition of HDAC enhances STAT acetylation, blocks NF-κB, and suppresses the renal inflammation and fibrosis in Npr1 haplotype male mice publication-title: Am. J. Physiol. Ren. Physiol. doi: 10.1152/ajprenal.00166.2017 – volume: 1802 start-page: 92 year: 2010 ident: ref_27 article-title: Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia publication-title: Biochimica Biophysica Acta doi: 10.1016/j.bbadis.2009.09.002 – volume: 52 start-page: 731 year: 2020 ident: ref_7 article-title: COVID-19: A new virus, but a familiar receptor and cytokine release syndrome publication-title: Immunity doi: 10.1016/j.immuni.2020.04.003 – volume: 6 start-page: 321 year: 2005 ident: ref_19 article-title: A pervasive role of ubiquitin conjugation in activation and termination of IkappaB kinase pathways publication-title: EMBO Rep. doi: 10.1038/sj.embor.7400380 – volume: 12 start-page: 216 year: 2017 ident: ref_22 article-title: Oxidative stress and apoptosis after acute respiratory hypoxia and reoxygenation in rat brain publication-title: Redox Biol. doi: 10.1016/j.redox.2017.02.014 – volume: 74 start-page: 29 year: 2005 ident: ref_51 article-title: The Biochemistry of Parkinson’s Disease publication-title: Annu. Rev. Biochem. doi: 10.1146/annurev.biochem.74.082803.133400 – volume: 59 start-page: 13 year: 2000 ident: ref_15 article-title: Oxidative stress and nuclear factor-kappaB activation: A reassessment of the evidence in the light of recent discoveries publication-title: Biochem. Pharmacol. doi: 10.1016/S0006-2952(99)00296-8 – volume: 71 start-page: 146 year: 2014 ident: ref_24 article-title: Acute hypoxia produces a superoxide burst in cells publication-title: Free Radic. Biol. Med. doi: 10.1016/j.freeradbiomed.2014.03.011 – volume: 48 start-page: 377 year: 2010 ident: ref_38 article-title: Oxidants induce alternative splicing of α-synuclein: Implications for Parkinson’s disease publication-title: Free Radic. Biol. Med. doi: 10.1016/j.freeradbiomed.2009.10.045 – volume: 65 start-page: 135 year: 2001 ident: ref_33 article-title: Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: Contribution to the apoptotic theory in Parkinson’s disease publication-title: Prog. Neurobiol. doi: 10.1016/S0301-0082(01)00003-X – volume: 74 start-page: 1384 year: 2000 ident: ref_43 article-title: Interaction among mitochondria, mitogen-activated protein kinases, and nuclear factor-kappaB in cellular models of Parkinson’s disease publication-title: J. Neurochem. doi: 10.1046/j.1471-4159.2000.0741384.x – volume: 53 start-page: 66 year: 2020 ident: ref_6 article-title: COVID-19: Pathogenesis, cytokine storm and therapeutic potential of interferons publication-title: Cytokine Growth Factor Rev. doi: 10.1016/j.cytogfr.2020.05.002 – volume: 60 start-page: 1 year: 2013 ident: ref_65 article-title: DJ-1 facilitates the interaction between STAT1 and its phosphatase, SHP-1, in brain microglia and astrocytes: A novel anti-inflammatory function of DJ-1 publication-title: Neurobiol. Dis. doi: 10.1016/j.nbd.2013.08.007 – volume: 16 start-page: 1215 year: 2015 ident: ref_59 article-title: PARP9-DTX3L ubiquitin ligase targets host histone H2BJ and viral 3C protease to enhance interferon signaling and control viral infection publication-title: Nature Immunol. doi: 10.1038/ni.3279 – volume: 175 start-page: 303 year: 2002 ident: ref_30 article-title: Modeling Parkinson’s disease in rats: An evaluation of 6-OHDA lesions of the Nigrostriatal pathway publication-title: Exp. Neurol. doi: 10.1006/exnr.2002.7891 – volume: 24 start-page: 103 year: 2015 ident: ref_42 article-title: Mitochondrial dysfunction in Parkinson’s disease publication-title: Exp. Neurobiol. doi: 10.5607/en.2015.24.2.103 – volume: 24 start-page: 757 year: 2013 ident: ref_56 article-title: Hyperphosphorylation of CREB induced by 6 OHDA treatment in human dopaminergic neurons: A kinetic study of distribution of tCREB and pCREB following oxidative stress publication-title: Neuroreport doi: 10.1097/WNR.0b013e328364d616 – volume: 553 start-page: 72 year: 2013 ident: ref_71 article-title: Protective effect of SIRT1 on toxicity of microglial-derived factors induced by LPS to PC12 cells via the p53-caspase-3-dependent apoptotic pathway publication-title: Neurosci. Lett. doi: 10.1016/j.neulet.2013.08.020 – volume: 63 start-page: 784 year: 2003 ident: ref_74 article-title: Nuclear translocation of nuclear transcription factor-kappa B by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors leads to transcription of p53 and cell death in dopaminergic neurons publication-title: Mol. Pharmacol. doi: 10.1124/mol.63.4.784 – ident: ref_12 doi: 10.3390/v12060646 – volume: 6 start-page: 372 year: 2015 ident: ref_23 article-title: Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved? publication-title: Redox Biol. doi: 10.1016/j.redox.2015.08.016 – volume: 296 start-page: R1829 year: 2009 ident: ref_35 article-title: D1/D2-dopamine receptor agonist dihydrexidine stimulates inspiratory motor output and depresses medullary expiratory neurons publication-title: Am. J. Physiol. Regul. Integr. Comp. Physiol. doi: 10.1152/ajpregu.00057.2009 – volume: 9 start-page: 91 year: 2015 ident: ref_40 article-title: Oxidative stress and Parkinson’s disease publication-title: Front. Neuroanat. doi: 10.3389/fnana.2015.00091 – volume: 579 start-page: 270 year: 2020 ident: ref_4 article-title: A pneumonia outbreak associated with a new coronavirus of probable bat origin publication-title: Nature doi: 10.1038/s41586-020-2012-7 – volume: 395 start-page: 497 year: 2020 ident: ref_2 article-title: Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China publication-title: Lancet doi: 10.1016/S0140-6736(20)30183-5 – volume: 27 start-page: 41 year: 2019 ident: ref_52 article-title: Shikonin exerts cytotoxic effects in human colon cancers by inducing apoptotic cell death via the endoplasmic reticulum and mitochondria-mediated pathways publication-title: Biomol. Ther. doi: 10.4062/biomolther.2018.047 – volume: 27 start-page: 1868 year: 2007 ident: ref_48 article-title: Parkin mediates neuroprotection through activation of IkappaB kinase/nuclear factor-kappa B signalling publication-title: J. Neurosci. doi: 10.1523/JNEUROSCI.5537-06.2007 – volume: 56 start-page: 862 year: 2015 ident: ref_13 article-title: Jak1/Stat3 is an upstream signaling of NF-κB activation in Helicobacter pylori-induced IL-8 production in gastric epithelial AGS cells publication-title: Yonsei Med J. doi: 10.3349/ymj.2015.56.3.862 – volume: 14 start-page: 4431 year: 2017 ident: ref_39 article-title: Tectorigenin attenuates the MPP+-induced SH-SY5Y cell damage, indicating a potential beneficial role in Parkinson’s disease by oxidative stress inhibition publication-title: Exp. Ther. Med. – ident: ref_68 doi: 10.1101/cshperspect.a009365 – volume: 58 start-page: 221 year: 2004 ident: ref_75 article-title: Quinone formation as dopaminergic neuron-specific oxidative stress in the pathogenesis of sporadic parkinson’s disease and neurotoxin-induced parkinsonism publication-title: Acta Medica Okayama – volume: 292 start-page: 329 year: 1995 ident: ref_34 article-title: Inhibition of mitochondrial complexes I and IV by 6-hydroxydopamine publication-title: Eur. J. Pharmacol. – volume: 42 start-page: 288 year: 2007 ident: ref_14 article-title: Reactive oxygen species in in vitro pesticide-induced neuronal cell (SH-SY5Y) cytotoxicity: Role of NFκB and caspase-3 publication-title: Free Radic. Biol. Med. doi: 10.1016/j.freeradbiomed.2006.10.047 – volume: 7 start-page: 12849 year: 2016 ident: ref_58 article-title: PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation publication-title: Nat. Commun. doi: 10.1038/ncomms12849 |
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| Title | COVID-19 and Parkinson’s Disease: Shared Inflammatory Pathways Under Oxidative Stress |
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