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Amyloid formation and Cytotoxicity
Primary sources and mechanisms of the amyloid-induced cellular toxicity
are topics of a large debate, in particular addressing the question of
whether prefibrillar oligomers and rather than fibrils are the prime toxic
agents. A number of studies indicate that fibrils are harmless to the
cells and they may represent an escape route for smaller, more toxic aggregates.
Conversely , there are also experimental evidences demonstrating the neurotoxicity
and cytotoxicity of amyloid fibrils formed from different proteins. The
structural definition of the cytotoxic species is complicated by the polymorphism
of amyloid fibrils arising by multiple aggregation pathways promoted in
different conditions such as aggregated species rising from the same protein
but characterized by distinct morphologies (e.g. twisted or parallel assemblies
of protofibrils) exhibiting significantly different behaviours in cell
cultures. Moreover, it is important to focus the attention on the recently
suggested idea that not only a single uniform species but rather a continuum
of cross-β-sheet containing aggregates induce cell death this may
shed new light on the evidences indicating that the behavior of cells
in culture treated with destabilised non-pathogenic proteins show analogies
with cells in pathologic conditions.
This indication, together with the observation that the oligomers
and fibrils are characterized by common structural features suggests that
common mechanisms for cytotoxicity could exist and have to be perused
in common interactions involved in aggregation. Those cytotoxic properties
are likely to arise from the exposure of internal regions due to conformational
changes occurring during aggregation. The detailed comprehension of the
cytotoxicity mechanisms and of the role of intermediate species can only
be achieved by kinetic observation of aggregation processes simultaneously
with the observation of their effect on cells. In this context, studies
on model proteins in different conditions are required to explore the
generality of these observations.
List of related papers
- V. Vetri, R. Carrotta, P. Picone,
M. Di Carlo and V. Militello,
Biochim. Biophys. Acta – Protein & Proteomics 1804, (2010)
173-183: "Concanavalin A aggregation and toxicity on cell cultures"
- V. Vetri, G. Ossato, V. Militello,
M. A. Digman, M. Leone and E. Gratton,
Biophysical Journal 96 (3) Supplement 1, (2009) 88a : "Detecting Protein Aggregation on Cells Surface: Concanavalin
A Oligomers Formation "
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