id:"swepub:oai:lup.lub.lu.se:67c1f607-cea0-4184-840d-c206b319c032"
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- Cheng, FangLund University,Lunds universitet,Glykobiologigruppen,Forskargrupper vid Lunds universitet,Glycobiology,Lund University Research Groups (author)
The cyanobacterial neurotoxin β-N-methylamino-L-alanine prevents addition of heparan sulfate to glypican-1 and increases processing of amyloid precursor protein in dividing neuronal cells
- Article/chapterEnglish2019
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- Elsevier BV,2019
- 10 s.
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- LIBRIS-ID:oai:lup.lub.lu.se:67c1f607-cea0-4184-840d-c206b319c032
- https://lup.lub.lu.se/record/67c1f607-cea0-4184-840d-c206b319c032URI
- https://doi.org/10.1016/j.yexcr.2019.03.041DOI
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- Language:English
- Summary in:English
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- The neurotoxin β-N-methylamino-L-alanine replaces L-serine in proteins and produces Alzheimer-like pathology. In proteoglycans, e.g. glypican-1, this should preclude substitution with heparan sulfate chains. Reduced release of heparan sulfate should increase β-secretase activity and processing of amyloid precursor protein. Cultured cells were treated with β-N-methylamino-L-alanine during the growth-phase and the effect on heparan sulfate substitution and amyloid precursor protein processing was evaluated using antibodies specific for heparan sulfate, the N- and C-termini of the C-terminal fragment of β-cleaved amyloid precursor protein, and amyloid beta followed by immunofluorescence microscopy, flow cytometry or SDS-PAGE. Mouse fibroblasts, N2a neuroblastoma cells and human neural stem cells released less heparan sulfate when grown in the presence of β-N-methylamino-L-alanine. Cells expressing a recombinant, anchor-less glypican-1 secreted heparan sulfate-deficient glypican-1. There was increased processing of amyloid precursor protein in N2a cells when grown in the presence of the neurotoxin. The degradation products accumulated in cytoplasmic clusters. Secretion of amyloid beta increased approx. 3-fold. Human neural stem cells also developed cytoplasmic clusters containing degradation products of amyloid precursor protein. When non-dividing mouse N2a cells or cortical neurons were exposed to β-N-methylamino-L-alanine there was no effect on heparan sulfate substitution in glypican-1 or on amyloid precursor protein processing.
Subject headings and genre
- MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Cell- och molekylärbiologi hsv//swe
- MEDICAL AND HEALTH SCIENCES Basic Medicine Cell and Molecular Biology hsv//eng
- Alzheimer's disease
- Amyloid precursor protein
- Glypican-1
- Heparan sulfate
- Neuronal cells
- Neurotoxin
Added entries (persons, corporate bodies, meetings, titles ...)
- Fransson, Lars ÅkeLund University,Lunds universitet,Glykobiologigruppen,Forskargrupper vid Lunds universitet,Glycobiology,Lund University Research Groups(Swepub:lu)medk-laf (author)
- Mani, KatrinLund University,Lunds universitet,Glykobiologigruppen,Forskargrupper vid Lunds universitet,Glycobiology,Lund University Research Groups(Swepub:lu)medk-kma (author)
- GlykobiologigruppenForskargrupper vid Lunds universitet (creator_code:org_t)
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- In:Experimental Cell Research: Elsevier BV379:2, s. 172-1810014-4827
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