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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Aluminum affects neural phenotype determination of embryonic neural progenitor cells

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Reichert, Karine P. [1] ; Schetinger, Maria Rosa C. [1] ; Pillat, Micheli M. [2, 1] ; Bottari, Nathieli B. [1] ; Palma, Tais V. [1] ; Gutierres, Jessie M. [3] ; Ulrich, Henning [2] ; Andrade, Cinthia M. [1] ; Exley, Christopher [4] ; Morsch, Vera M. M. [1]
Total Authors: 10
[1] Fed Univ Santa Maria UFSM, Dept Biochem & Mol Biol, Postgrad Program Toxicol Biochem, Lab Toxicol Enzymol, BR-97105900 Santa Maria, RS - Brazil
[2] Univ Sao Paulo, Inst Chem, Dept Biochem, Sao Paulo, SP - Brazil
[3] Fed Univ Hlth Sci Porto Alegre UFCSPA, Lab Res Pathol, Porto Alegre, RS - Brazil
[4] Keele Univ, Birchall Ctr, Lennard Jones Labs, Keele ST5 5BG, Staffs - England
Total Affiliations: 4
Document type: Journal article
Source: ARCHIVES OF TOXICOLOGY; v. 93, n. 9, p. 2515-2524, SEP 2019.
Web of Science Citations: 1

Aluminum (Al) is a neurotoxin and is associated with the etiology of neurodegenerative diseases, such as Alzheimer's disease (AD). The Al-free ion (Al3+) is the biologically reactive and toxic form. However, the underlying mechanisms of Al toxicity in the brain remain unclear. Here, we evaluated the effects of Al3+ (in the chloride form-AlCl3) at different concentrations (0.1-100 mu M) on the morphology, proliferation, apoptosis, migration and differentiation of neural progenitor cells (NPCs) isolated from embryonic telencephalons, cultured as neurospheres. Our results reveal that Al3+ at 100 mu M reduced the number and diameter of neurospheres. Cell cycle analysis showed that Al3+ had a decisive function in proliferation inhibition of NPCs during neural differentiation and induced apoptosis on neurospheres. In addition, 1 mu M Al3+ resulted in deleterious effects on neural phenotype determination. Flow cytometry and immunocytochemistry analysis showed that Al3+ promoted a decrease in immature neuronal marker beta 3-tubulin expression and an increase in co-expression of the NPC marker nestin and glial fibrillary acidic protein. Thus, our findings indicate that Al3+ caused cellular damage and reduced proliferation and migration, resulting in global inhibition of NPC differentiation and neurogenesis. (AU)

FAPESP's process: 15/19478-3 - Role of kinin-B2 receptor in pathogenesis and progression of familial Alzheimer's Disease: from neurogenesis and immune response to cognition
Grantee:Micheli Mainardi Pillat
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 12/50880-4 - Stem cells: from basic studies of kinin and purinergic receptor roles towards therapeutical applications
Grantee:Alexander Henning Ulrich
Support type: Research Projects - Thematic Grants