In the present study we performed ultrastructural dissection of cell-to-cell communication in vitro using an experimental model of glioblastoma multiforme. This experimental approach was combined with immunocytochemistry and staining for glycated end products. Evidence was provided showing an increased amount of misfolded proteins including prion protein and alpha synuclein which are released in the form of glycated compounds

BARTALUCCI, ALESSIA

FERRUCCI, MICHELA

FORNAI, FRANCESCO

FULCERI, FEDERICA

GESI, MARCO

NATALE, GIANFRANCO

RUFFOLI, RICCARDO

RYSKALIN, LARISA

SOLDANI, PAOLA

Intercellular communication is a physiological mechanism underlying cellular and systemic homeostasis. This occurs either through direct cell to cell contact (e.g. trogocytosis and tunneling nanotubes) or it involves vesicles secretion (e.g. endosome- derived exosome and microvesicles) (1,2). The release of extracellular vesicles is recruited in physiological processes while it plays a crucial role in protecting cells from accumulation of dangerous or waste compounds. Recent evidence suggests that altered intercellular communication of misfolded proteins is involved in tumors and neurodegeneration as well, thus posing cell-to-cell communication as an unconventional mechanism of disease spreading (3,4). In the present study we performed ultrastructural dissection of cell-to-cell communication in vitro using an experimental model of Glioblastoma Multiforme (GBM). Ultrastructural analysis was carried out by using transmission electron microscopy (TEM), which is the gold standard for vesicles detection, identification and size determination. This experimental approach was combined with immunocytochemistry and staining for glycated end products. Evidence is provided here showing increased amount of misfolded proteins including prion protein and alpha synuclein which are released in the form of glycated compounds. Release of glycated misfolded proteins can be modulated by altering specific protein clearing pathways. These studies set the stage for further investigations into multiple roles of cell-to-cell communication in neurodegeneration and disease progression

Ryskalin, Larisa

Ferrucci, Michela

Fulceri, Federica

Bartalucci, Alessia

Natale, Gianfranco

Ruffoli, Riccardo

Soldani, Paola

Gesi, Marco

Fornai, Francesco

Firenze University Press: E-Journals

IJAE 
Vo l .  120 ,  n .  1  (Supp lem ent) :  18 8 ,  2015
© 2015 Firenze University Press 
ht tp://www.fupress .com/ijae
ITALIAN JOURNAL OF ANATOMY AND EMBRYOLOGY
Altered intercellular diffusion of misfolded proteins in 
neuroglia 
Larisa Ryskalin, Michela Ferrucci, Federica Fulceri, Alessia Bartalucci, Gianfranco Natale, Riccardo 
Ruffoli, Paola Soldani, Marco Gesi, Francesco Fornai
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, 
Italy
Intercellular communication is a physiological mechanism underlying cellular 
and systemic homeostasis. This occurs either through direct cell to cell contact (e.g. 
trogocytosis and tunneling nanotubes) or it involves vesicles secretion (e.g. endo-
some-derived exosome and microvesicles) (1,2). The release of extracellular vesicles 
is recruited in physiological processes while it plays a crucial role in protecting cells 
from accumulation of dangerous or waste compounds. Recent evidence suggests that 
altered intercellular communication of misfolded proteins is involved in tumors and 
neurodegeneration as well, thus posing cell-to-cell communication as an unconven-
tional mechanism of disease spreading (3,4). In the present study we performed ultras-
tructural dissection of cell-to-cell communication in vitro using an experimental model 
of Glioblastoma Multiforme (GBM). Ultrastructural analysis was carried out by using 
transmission electron microscopy (TEM), which is the gold standard for vesicles detec-
tion, identification and size determination. This experimental approach was combined 
with immunocytochemistry and staining for glycated end products. Evidence is pro-
vided here showing increased amount of misfolded proteins including prion protein 
and alpha synuclein which are released in the form of glycated compounds. Release 
of glycated misfolded proteins can be modulated by altering specific protein clearing 
pathways. These studies set the stage for further investigations into multiple roles of 
cell-to-cell communication in neurodegeneration and disease progression.
References
 [1] Ratajczak et al. (2006) Membrane-derived microvesicles: Important and underappreciated media-
tors of cell-to-cell communication. Leukemia 20: 1487-1495. 
[2] Gerdes et al. (2007) Tunneling nanotubes: a new route for the exchange of components between 
animal cells. FEBS Lett 581: 2194-2201.
[3] Kahlert et al. (2013) Exosomes in tumor microenvironment influence cancer progression and 
metastasis. J Mol Med (Berl), 91: 431-437.
[4] Lai et al. (2012) Role of exosomes/microvesicles in the nervous system and use in emerging thera-
pies. Front Physiol 3: 228. 
Keywords
Cell-to-cell communication; ultrastructure; electron microscopy; U87MG.


Altered intercellular diffusion of misfolded proteins in neuroglia

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Altered intercellular diffusion of misfolded proteins in neuroglia.

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Altered intercellular diffusion of misfolded proteins in neuroglia.

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