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Inhibition of lysosomal functions reduces proteasomal activity

Qiao, Liyan, Zhang, Jianhua·2009·Neuroscience Letters
DOI 10.1016/j.neulet.2009.03.085
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Abstract

Protein accumulation and aggregation are signatures of several major neurodegenerative diseases. Proteasomal- and lysosomal-mediated protein degradation pathways are the two major pathways for intracellular protein degradation. Cross-regulation between these two pathways may be important for protein homeostasis. Pharmacological inhibition of proteasomal activities has been shown to up-regulate the levels of lysosomal enzymes. To determine whether the reverse regulatory mechanism also occurs in the cell, we investigated the effects of inhibition of lysosomal function on proteasomal activities. We found that rather than up-regulating proteasomal activities in response to lysosomal disruptors, reduced lysosomal function reduces proteasomal functions, indicating a lack of compensatory up-regulation of proteasomal functions. Inhibition of lysosomal or proteasomal activities led to higher levels of chaperone heat shock cognate protein Hsc70, suggesting an attempt to compensate protein degradation deficiency by enhancing chaperone-mediated autophagy.

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Research works printed but not linked: 56

  1. Anderson, 2005, Loss of Usp14 results in reduced levels of ubiquitin in ataxia mice, J. Neurochem., 95, 724, 10.1111/j.1471-4159.2005.03409.x · DOI
  2. Anglade, 1997, Apoptosis and autophagy in nigral neurons of patients with Parkinson's disease, Histol. Histopathol., 12, 25
  3. Bandhyopadhyay, 2006, Chaperone-mediated autophagy in aging and neurodegeneration: lessons from alpha-synuclein, Exp. Gerontol.
  4. Barrachina, 2006, Reduced ubiquitin C-terminal hydrolase-1 expression levels in dementia with Lewy bodies, Neurobiol. Dis., 22, 265, 10.1016/j.nbd.2005.11.005 · DOI
  5. Bennett, 1999, Degradation of alpha-synuclein by proteasome, J. Biol. Chem., 274, 33855, 10.1074/jbc.274.48.33855 · DOI · Paper page
  6. Berger, 2006, Rapamycin alleviates toxicity of different aggregate-prone proteins, Hum. Mol. Genet., 15, 433, 10.1093/hmg/ddi458 · DOI · Paper page
  7. Cantuti-Castelvetri, 2005, Alpha-synuclein and chaperones in dementia with Lewy bodies, J. Neuropathol. Exp. Neurol., 64, 1058, 10.1097/01.jnen.0000190063.90440.69 · DOI
  8. Cao, 2005, Torsin-mediated protection from cellular stress in the dopaminergic neurons of Caenorhabditis elegans, J. Neurosci., 25, 3801, 10.1523/JNEUROSCI.5157-04.2005 · DOI
  9. Cataldo, 1994, Lysosomal abnormalities in degenerating neurons link neuronal compromise to senile plaque development in Alzheimer disease, Brain Res., 640, 68, 10.1016/0006-8993(94)91858-9 · DOI · Paper page
  10. Cooper, 2006, Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models, Science, 313, 324, 10.1126/science.1129462 · DOI
  11. Cuervo, 2000, Unique properties of lamp2a compared to other lamp2 isoforms, J. Cell Sci. 113 Pt, 24, 4441, 10.1242/jcs.113.24.4441 · DOI
  12. Dauer, 2002, Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTP, Proc. Natl. Acad. Sci. U.S.A., 99, 14524, 10.1073/pnas.172514599 · DOI
  13. Dean, 1979, Lysosomes and protein degradation, Ciba Found. Symp., 139
  14. Ding, 2007, Linking of autophagy to ubiquitin-proteasome system is important for the regulation of endoplasmic reticulum stress and cell viability, Am. J. Pathol., 171, 513, 10.2353/ajpath.2007.070188 · DOI · Paper page
  15. Ding, 2008, Sorting, recognition and activation of the misfolded protein degradation pathways through macroautophagy and the proteasome, Autophagy, 4, 141, 10.4161/auto.5190 · DOI
  16. Drolet, 2004, Mice lacking alpha-synuclein have an attenuated loss of striatal dopamine following prolonged chronic MPTP administration, Neurotoxicology, 25, 761, 10.1016/j.neuro.2004.05.002 · DOI
  17. Fujita, 2007, Two endoplasmic reticulum-associated degradation (ERAD) systems for the novel variant of the mutant dysferlin: ubiquitin/proteasome ERAD(I) and autophagy/lysosome ERAD(II), Hum. Mol. Genet., 16, 618, 10.1093/hmg/ddm002 · DOI · Paper page
  18. Gao, 2008, Neuroinflammation and oxidation/nitration of alpha-synuclein linked to dopaminergic neurodegeneration, J. Neurosci., 28, 7687, 10.1523/JNEUROSCI.0143-07.2008 · DOI
  19. Giasson, 2002, Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein, Neuron, 34, 521, 10.1016/S0896-6273(02)00682-7 · DOI · Paper page
  20. Hara, 2006, Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice, Nature, 441, 885, 10.1038/nature04724 · DOI · Paper page
  21. Hayashita-Kinoh, 2006, Down-regulation of alpha-synuclein expression can rescue dopaminergic cells from cell death in the substantia nigra of Parkinson's disease rat model, Biochem. Biophys. Res. Commun., 341, 1088, 10.1016/j.bbrc.2006.01.057 · DOI
  22. Hunter, 2007, Ubiquitin-proteasome system alterations in a striatal cell model of Huntington's disease, J. Neurosci. Res., 85, 1774, 10.1002/jnr.21287 · DOI
  23. Ii, 1997, Immunocytochemical co-localization of the proteasome in ubiquitinated structures in neurodegenerative diseases and the elderly, J. Neuropathol. Exp. Neurol., 56, 125, 10.1097/00005072-199702000-00002 · DOI
  24. Kahle, 2008, Alpha-synucleinopathy models and human neuropathology: similarities and differences, Acta Neuropathol., 115, 87, 10.1007/s00401-007-0302-x · DOI
  25. Klivenyi, 2006, Mice lacking alpha-synuclein are resistant to mitochondrial toxins, Neurobiol. Dis., 21, 541, 10.1016/j.nbd.2005.08.018 · DOI
  26. Komatsu, 2006, Loss of autophagy in the central nervous system causes neurodegeneration in mice, Nature, 441, 880, 10.1038/nature04723 · DOI · Paper page
  27. Komatsu, 2007, Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice, Cell, 131, 1149, 10.1016/j.cell.2007.10.035 · DOI · Paper page
  28. Lee, 2004, Clearance of alpha-synuclein oligomeric intermediates via the lysosomal degradation pathway, J. Neurosci., 24, 1888, 10.1523/JNEUROSCI.3809-03.2004 · DOI · Paper page
  29. Lee, 2006, Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery, Neuron, 52, 33, 10.1016/j.neuron.2006.09.026 · DOI
  30. Leverenz, 2007, Proteomic identification of novel proteins in cortical lewy bodies, Brain Pathol., 17, 139, 10.1111/j.1750-3639.2007.00048.x · DOI
  31. Li, 2004, Stabilization of alpha-synuclein protein with aging and familial parkinson's disease-linked A53T mutation, J. Neurosci., 24, 7400, 10.1523/JNEUROSCI.1370-04.2004 · DOI
  32. Martinez-Vicente, 2008, Dopamine-modified alpha-synuclein blocks chaperone-mediated autophagy, J. Clin. Invest., 10.1172/JCI32806 · DOI
  33. Masliah, 2000, Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders, Science, 287, 1265, 10.1126/science.287.5456.1265 · DOI
  34. Massey, 2006, Consequences of the selective blockage of chaperone-mediated autophagy, Proc. Natl. Acad. Sci. U.S.A., 103, 5805, 10.1073/pnas.0507436103 · DOI · Paper page
  35. Massey, 2006, Chaperone-mediated autophagy in aging and disease, Curr. Top. Dev. Biol., 73, 205, 10.1016/S0070-2153(05)73007-6 · DOI · Paper page
  36. McLean, 2001, Alpha-synuclein-enhanced green fluorescent protein fusion proteins form proteasome sensitive inclusions in primary neurons, Neuroscience, 104, 901, 10.1016/S0306-4522(01)00113-0 · DOI
  37. McNaught, 2003, Altered proteasomal function in sporadic Parkinson's disease, Exp. Neurol., 179, 38, 10.1006/exnr.2002.8050 · DOI · Paper page
  38. McNaught, 2002, Proteasome inhibition causes nigral degeneration with inclusion bodies in rats, Neuroreport, 13, 1437, 10.1097/00001756-200208070-00018 · DOI
  39. McNaught, 2001, Proteasomal function is impaired in substantia nigra in Parkinson's disease, Neurosci. Lett., 297, 191, 10.1016/S0304-3940(00)01701-8 · DOI · Paper page
  40. McNaught, 2002, Aggresome-related biogenesis of Lewy bodies, Eur. J. Neurosci., 16, 2136, 10.1046/j.1460-9568.2002.02301.x · DOI
  41. Meredith, 2002, Lysosomal malfunction accompanies alpha-synuclein aggregation in a progressive mouse model of Parkinson's disease, Brain Res., 956, 156, 10.1016/S0006-8993(02)03514-X · DOI
  42. Nakamura, 1989, Lysosome instability in aged rat brain, Neurosci. Lett., 97, 215, 10.1016/0304-3940(89)90166-3 · DOI
  43. Nixon, 2005, Extensive involvement of autophagy in Alzheimer disease: an immuno-electron microscopy study, J. Neuropathol. Exp. Neurol., 64, 113, 10.1093/jnen/64.2.113 · DOI · Paper page
  44. Nuber, 2008, Neurodegeneration and motor dysfunction in a conditional model of Parkinson's disease, J. Neurosci., 28, 2471, 10.1523/JNEUROSCI.3040-07.2008 · DOI
  45. Qiao, 2008, Lysosomal enzyme cathepsin D protects against alpha-synuclein aggregation and toxicity, Mol. Brain, 1, 17, 10.1186/1756-6606-1-17 · DOI
  46. Rideout, 2004, Involvement of macroautophagy in the dissolution of neuronal inclusions, Int. J. Biochem. Cell Biol., 36, 2551, 10.1016/j.biocel.2004.05.008 · DOI
  47. Rideout, 2002, Proteasomal inhibition-induced inclusion formation and death in cortical neurons require transcription and ubiquitination, Mol. Cell. Neurosci., 21, 223, 10.1006/mcne.2002.1173 · DOI
  48. Robertson, 2004, Developmental loss and resistance to MPTP toxicity of dopaminergic neurones in substantia nigra pars compacta of gamma-synuclein, alpha-synuclein and double alpha/gamma-synuclein null mutant mice, J. Neurochem., 89, 1126, 10.1111/j.1471-4159.2004.02378.x · DOI
  49. Sampathu, 2003, Ubiquitination of alpha-synuclein is not required for formation of pathological inclusions in alpha-synucleinopathies, Am. J. Pathol., 163, 91, 10.1016/S0002-9440(10)63633-4 · DOI
  50. Sarkar, 2007, Trehalose, a novel mTOR-independent autophagy enhancer, accelerates the clearance of mutant huntingtin and alpha-synuclein, J. Biol. Chem., 282, 5641, 10.1074/jbc.M609532200 · DOI · Paper page
  51. Sarkar, 2008, A rational mechanism for combination treatment of Huntington's disease using lithium and rapamycin, Hum. Mol. Genet., 17, 170, 10.1093/hmg/ddm294 · DOI
  52. Sarkar, 2006, Inositol and IP3 levels regulate autophagy: biology and therapeutic speculations, Autophagy, 2, 132, 10.4161/auto.2387 · DOI
  53. Shin, 2005, The co-chaperone carboxyl terminus of Hsp70-interacting protein (CHIP) mediates alpha-synuclein degradation decisions between proteasomal and lysosomal pathways, J. Biol. Chem., 280, 23727, 10.1074/jbc.M503326200 · DOI
  54. Singleton, 2003, Alpha-synuclein locus triplication causes Parkinson's disease, Science, 302, 841, 10.1126/science.1090278 · DOI · Paper page
  55. Tofaris, 2001, Alpha-synuclein metabolism and aggregation is linked to ubiquitin-independent degradation by the proteasome, FEBS Lett., 509, 22, 10.1016/S0014-5793(01)03115-5 · DOI · Paper page
  56. Vernace, 2007, Aging and regulated protein degradation: who has the UPPer hand?, Aging Cell, 10.1111/j.1474-9726.2007.00329.x · DOI · Paper page

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Metadata

Authors
Qiao, L., & Zhang, J.
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
2009-05
Volume
456
Issue
1
Pages
15-19
ISSN
0304-3940
DOI
10.1016/j.neulet.2009.03.085
Cited by
50
References
10
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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CoChat. (2026). Citation check: Inhibition of lysosomal functions reduces proteasomal activity. https://app.cochat.ai/papers/10.1016/j.neulet.2009.03.085
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Qiao, L., & Zhang, J. (2009). Inhibition of lysosomal functions reduces proteasomal activity. Neuroscience Letters. https://doi.org/10.1016/j.neulet.2009.03.085