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Activated α2Macroglobulin Increases β-Amyloid (25–35)-Induced Toxicity in LAN5 Human Neuroblastoma Cells

Fabrizi, C., Businaro, R., Lauro, G.M., Starace, G., Fumagalli, L.·1999·Experimental Neurology
DOI 10.1006/exnr.1998.6978
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Abstract

The presence of the alpha2macroglobulin receptor/low density lipoprotein receptor-related protein (alpha2Mr/LRP) and its ligands alpha2macroglobulin (alpha2M), apoliprotein E, and plasminogen activators was detected in senile plaques of Alzheimer's disease (AD). To explore a possible role of alpha2M in neurodegenerative processes occurring in AD, we analyzed the effect of alpha2M on Abeta 25-35-induced neurotoxicity. Treatment of LAN5 human neuroblastoma cells with 10 microM beta-amyloid peptide fragment 25-35 (Abeta 25-35) for 72 h resulted in a 50% decrease in cell viability as determined by MTT incorporation and cell counts. The addition of alpha2M to the culture medium of these cells did not determine any effect, but when the activated form alpha2M* was used a dose-dependent decrease in cell viability was observed, the maximum effect being reached at 140 and 280 nM. Moreover, treatment of LAN5 cells with alpha2M* in combination with Abeta 25-35 increased the neurotoxicity of the amyloid peptide by 25%. This neurotoxic effect of alpha2M* seems to be related to its capability to bind and inactivate TGFbeta in the culture medium, since it was mimicked by a TGFbeta neutralizing antibody. A possible involvement of receptor-mediated endocytosis was ruled out, since alpha2M receptor is not present on LAN5, as revealed by RT-PCR and Western blotting experiments. The presence of alpha2M* in amyloid deposits of Alzheimer's disease has been recently reported and a possible impairmen…

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Research works printed but not linked: 48

  1. Abraham, 1988, Immunochemical identification of the serine protease inhibitor α1, Cell, 52, 487, 10.1016/0092-8674(88)90462-X · DOI
  2. Aksenov, 1996, α1, Neurosci. Lett., 217, 117, 10.1016/0304-3940(96)13082-2 · DOI
  3. Barger, 1997, Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E, Nature, 388, 878, 10.1038/42257 · DOI · Paper page
  4. Barrett, 1981, α2, Methods Enzymol., 80, 737, 10.1016/S0076-6879(81)80056-0 · DOI
  5. Bauer, 1991, Interleukin-6 and α2, FEBS Lett., 285, 111, 10.1016/0014-5793(91)80737-N · DOI · Paper page
  6. Bjork, 1982, Evidence for similar conformational changes in α2, Biochem J., 207, 347
  7. Businaro, 1992, Synthesis and secretion of α2, Exp. Brain Res., 88, 213, 10.1007/BF02259144 · DOI
  8. Businaro, 1997, Modulation of the α2, J. Neuroimmunol., 72, 75, 10.1016/S0165-5728(96)00157-9 · DOI
  9. Cataldo, 1996, Colocalization of lysosomal hydrolase and β-amyloid in diffuse plaques of the cerebellum and striatum in Alzheimer's disease and Down's syndrome, J. Neuropathol. Exp. Neurol., 55, 704, 10.1097/00005072-199606000-00004 · DOI
  10. Cone, 1988, An improved method for purification of transforming growth factor, type beta, from platelets, Anal. Biochem., 168, 71, 10.1016/0003-2697(88)90011-5 · DOI
  11. Crookston, 1994, Classification of α2, J. Biol. Chem., 269, 1533, 10.1016/S0021-9258(17)42289-7 · DOI
  12. Danielpour, 1990, Differential inhibition of transforming growth factorβ122, J. Biol. Chem., 265, 6973, 10.1016/S0021-9258(19)39246-4 · DOI
  13. Dickson, 1997, The pathogenesis of senile plaques, Neuropathol. Exp. Neurol., 56, 321, 10.1097/00005072-199704000-00001 · DOI · Paper page
  14. Du, 1998, α2, J. Neurochem., 70, 1182, 10.1046/j.1471-4159.1998.70031182.x · DOI
  15. Fabrizi, 1994, Interferon γ up-regulates α2, J. Neuroimmunol., 53, 31, 10.1016/0165-5728(94)90061-2 · DOI
  16. Feige, 1996, Macroglobulin: A binding protein for Transforming Growth Factor-β and various cytokines, Horm. Res., 45, 227, 10.1159/000184793 · DOI
  17. Gitter, 1995, Amyloid peptide potentiates cytokine secretion by interleukin-1β-activated human astrocytoma cells, Proc. Natl. Acad. Sci. USA, 92, 10738, 10.1073/pnas.92.23.10738 · DOI
  18. Goodman, 1994, Secreted forms of β-amyloid precursor protein protect hippocampal neurons against amyloid β-peptide-induced oxidative injury, Exp. Neurol., 128, 1, 10.1006/exnr.1994.1107 · DOI
  19. Hansen, 1989, Re-examination and further development of a precise and rapid dye method for measuring cell growth/cell kill, J. Immunol. Meth., 119, 203, 10.1016/0022-1759(89)90397-9 · DOI
  20. Ii, 1993, Abnormal distribution of cathepsin proteinases and endogenous inhibitors (cystatins) in the hippocampus of patients with Alzheimer's disease, Virchows. Arch. A Pathol. Anat. Histopathol., 423, 185, 10.1007/BF01614769 · DOI
  21. Kawamata, 1993, Lactotransferrin immunocytochemistry in Alzheimer and normal human brain, Am. J. Pathol., 142, 1574
  22. Keramidas, 1991, Immunolocalization of transforming growth factor-β1, Endocrinology, 129, 517, 10.1210/endo-129-1-517 · DOI
  23. Kosik, 1992, Alzheimer's disease: A cell biological perspective, Science, 256, 780, 10.1126/science.1589757 · DOI
  24. Kounnas, 1995, LDL receptor-related protein, a multifunctional ApoE receptor, binds secreted β-amyloid precursor protein and mediates its degradation, Cell, 82, 331, 10.1016/0092-8674(95)90320-8 · DOI · Paper page
  25. Lampariello, 1994, Evaluation of the number of positive cells from flow cytometric immunoassays by mathematical modeling of cellular autofluorescence, Cytometry, 15, 294, 10.1002/cyto.990150404 · DOI
  26. Lysiak, 1995, α2, J. Biol. Chem., 270, 21919, 10.1074/jbc.270.37.21919 · DOI
  27. Mattson, 1997, Cellular signaling roles of TGFβ, TNFα and βApp in brain injury responses and Alzheimer's disease, Brain Res. Rev., 23, 47, 10.1016/S0165-0173(96)00014-8 · DOI
  28. Moestrup, 1992, Surface expression of the α2, Leukem. Res., 16, 227, 10.1016/0145-2126(92)90060-K · DOI
  29. Moestrup, 1994, The α2, Biochim. Biophys. Acta, 197, 197, 10.1016/0304-4157(94)90005-1 · DOI
  30. Mrak, 1995, Glial cytokines in Alzheimer's disease: Review and pathogenic implications, Hum. Pathol., 26, 816, 10.1016/0046-8177(95)90001-2 · DOI
  31. O'Connor-McCourt, 1987, Latent transforming growth factor-β in serum: a specific complex with α2, J. Biol. Chem., 262, 14090, 10.1016/S0021-9258(18)47909-4 · DOI
  32. Prehn, 1993, Transforming growth factor-β prevents glutamate neurotoxicity in rat neocortical cultures and protect mouse neocortex from ischemic injuryin vivo, J. Cerebral Blood Flow Metab., 13, 521, 10.1038/jcbfm.1993.67 · DOI
  33. Prehn, 1996, Protective effect of transforming growth factor-β1, Mol. Pharmacol., 49, 319
  34. Qiao, 1996, Degradation of amyloid β-protein by a serine protease-α2, J. Biol. Chem., 271, 8443, 10.1074/jbc.271.14.8443 · DOI
  35. Rebeck, 1993, Apolipoprotein E in sporadic Alzheimer's disease: allelic variation and receptor interactions, Neuron, 11, 575, 10.1016/0896-6273(93)90070-8 · DOI · Paper page
  36. Ren, 1996, Transforming growth factors-β protect primary rat hippocampal neuronal cultures from degeneration induced by β-amyloid peptide, Brain Res., 732, 16, 10.1016/0006-8993(96)00458-1 · DOI
  37. Scarpa, 1996, Transforming growth factor-β regulates differentiation and proliferation of human neuroblastoma, Exp. Cell Res., 229, 147, 10.1006/excr.1996.0352 · DOI
  38. Selkoe, 1993, Physiological production of the β-amyloid protein and the mechanism of Alzheimer's disease, Trends Neurosci., 16, 403, 10.1016/0166-2236(93)90008-A · DOI
  39. Smith, 1993, α1, Biochem. Biophys. Res. Commun., 193, 579, 10.1006/bbrc.1993.1663 · DOI
  40. Starkey, 1977, The degradation of articular collagen by neutrophil proteinases, Biochim. Biophys. Acta, 483, 386, 10.1016/0005-2744(77)90066-3 · DOI
  41. Strauss, 1992, Detection of interleukin-6 and α2, Lab. Invest., 66, 223
  42. Thal, 1997, The subunits of α22, Brain Res., 777, 223, 10.1016/S0006-8993(97)01021-4 · DOI
  43. Unsicker, 1991, Transforming growth factorβ isoforms in the adult rat central and peripheral nervous system, Neuroscience, 44, 613, 10.1016/0306-4522(91)90082-Y · DOI
  44. Van Der Wal, 1993, Transforming growth factor-β1, NeuroReport, 4, 69, 10.1097/00001756-199301000-00018 · DOI
  45. Van Gool, 1993, α2, Neurobiol. Aging, 14, 233, 10.1016/0197-4580(93)90006-W · DOI
  46. Webb, 1997, Chemical modification of α2, FEBS, 410, 249, 10.1016/S0014-5793(97)00598-X · DOI
  47. Willis, 1987, Amine accumulation in Parkinson's disease and other disorders, Neurosci. Biobehav. Rev., 11, 97, 10.1016/S0149-7634(87)80004-0 · DOI
  48. Wolf, 1994, Neurotrophin binding to human α2, Biochemistry, 33, 11270, 10.1021/bi00203a024 · DOI

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Metadata

Authors
Fabrizi, C., Businaro, R., Lauro, G. M., Starace, G., & Fumagalli, L.
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
1999-02
Volume
155
Issue
2
Pages
252-259
ISSN
0014-4886
DOI
10.1006/exnr.1998.6978
Cited by
14
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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