Effect of Some Growth Factors on Tissue Transglutaminase Overexpression Induced by β-Amyloid in Olfactory Ensheathing Cells

Autor: Agata Campisi, Giuseppina Raciti, Roberta Bonfanti, Rosalia Pellitteri, Mariacristina Ferrara, Maria Teresa Cambria, Michela Spatuzza
Rok vydání: 2016
Předmět:
Enzymologic
0301 basic medicine
Tissue transglutaminase
Basic fibroblast growth factor
Wistar
Stress conditions
chemistry.chemical_compound
0302 clinical medicine
Neurotrophic factors
Glial cell line-derived neurotrophic factor
Cells
Cultured
Beta-amyloid fragments
Cultured
Olfactory Ensheathing Cells
Tissue Transglutaminase
Beta Amyloid Fragments
Stress Conditions
Growth Factors
Neurotoxicity
medicine.diagnostic_test
biology
Cell Differentiation
Olfactory Bulb
Neurology
Intercellular Signaling Peptides and Proteins
Growth factors
Intracellular
Cell Survival
Cells
Neuroscience (miscellaneous)
Gene Expression Regulation
Enzymologic
03 medical and health sciences
Cellular and Molecular Neuroscience
Western blot
GTP-Binding Proteins
medicine
Animals
Protein Glutamine gamma Glutamyltransferase 2
Viability assay
Rats
Wistar
Amyloid beta-Peptides
Transglutaminases
Newborn
Molecular biology
Peptide Fragments
Rats
030104 developmental biology
Gene Expression Regulation
Animals
Newborn
chemistry
Olfactory ensheathing cells
biology.protein
Olfactory ensheathing glia
030217 neurology & neurosurgery
Zdroj: Molecular neurobiology 54 (2017): 6785–6794. doi:10.1007/s12035-016-0152-4
info:cnr-pdr/source/autori:Pellitteri R.; Bonfanti R.; Spatuzza M.; Cambria M.T.; Ferrara M.; Raciti G.; Campisi A./titolo:Effect of Some Growth Factors on Tissue Transglutaminase Overexpression Induced by ?-Amyloid in Olfactory Ensheathing Cells/doi:10.1007%2Fs12035-016-0152-4/rivista:Molecular neurobiology/anno:2017/pagina_da:6785/pagina_a:6794/intervallo_pagine:6785–6794/volume:54
ISSN: 1559-1182
0893-7648
DOI: 10.1007/s12035-016-0152-4
Popis: Herein, we assessed in a particular glial cell type, called olfactory ensheathing cells (OECs), the effect of some growth factors (GFs) on tissue transglutaminase (TG2) overexpression induced by amyloid-beta (Aβ) with native full-length peptide 1-42 or by fragments, 25-35 or 35-25, as control. Previously, we demonstrated that TG2 overexpression induced by some stressors was down-regulated by GFs exposure in OECs. To monitor cell viability, an MTT test was used, while TG2 expression was examined using immunocytochemical and Western blot analysis. We also considered the involvement of the TG2-mediated apoptotic pathway. Vimentin expression was evaluated as well. Reactive oxygen species and reduced glutathione levels were utilized to test the oxidative intracellular status. Lactate dehydrogenase released into the medium, as a marker of necrotic cell death, was evaluated. We found that in OECs exposed to Aβ(1-42) or Aβ(25-35) for 24 h, TG2 expression increased, and we observed that the protein appeared prevalently localized in the cytosol. The pre-treatment with GFs, basic fibroblast growth factor (bFGF) or glial-derived neurotrophic factor (GDNF), down-regulated the TG2 level, which was prevalently limited to the nuclear compartment. Vimentin expression and caspase cleavage showed a significant enhancement in Aβ(1-42) and Aβ(25-35) exposed cells. The pre-treatment with bFGF or GDNF was able to restore the levels of the proteins to control values, and the intracellular oxidative status modified by the exposure to Aβ(1-42) or Aβ(25-35). Our data suggest that both bFGF or GDNF could be an innovative mechanism to contrast TG2 expression, which plays a key role in Alzheimer's disease.
Databáze: OpenAIRE
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