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Nanoparticulate TiO2-mediated inhibition of the Wnt signaling pathway causes dendritic development disorder in cultured rat hippocampal neurons.
- Source :
- Journal of Biomedical Materials Research, Part A; Aug2017, Vol. 105 Issue 8, p2139-2149, 11p
- Publication Year :
- 2017
-
Abstract
- Titanium dioxide nanoparticles (TiO<subscript>2</subscript> NPs) are increasingly used in daily life, in industry, and in environmental clearing, but their potential neurodevelopmental toxicity has been highly debated. In this study, we explored whether TiO<subscript>2</subscript> NPs inhibited development of dendritic morphology and identified possible molecular mechanisms associated with this inhibition in primary cultured rat hippocampal neurons. Results showed that TiO<subscript>2</subscript> NPs decreased neurite length, the number of branches and the spine density, and impaired mitochondrial function in the developing neurons. Furthermore, TiO<subscript>2</subscript> NPs significantly reduced the expression of several proteins involved in canonical Wnt3a/β-catenin signaling including Wnt3a, β-catenin, p-GSK-3β, and CyclinD1 and conversely, elevated GSK-3β expression. In addition to altering expression of proteins involved in canonical Wnt3a/β-catenin signaling, TiO<subscript>2</subscript> NPs decreased expression of proteins invovled in non-canonical Wnt signaling, including, MKLP1, CRMP3, ErbB4, and KIF17. Taken together, these results indicate that suppression of dendritic development caused by TiO<subscript>2</subscript> NPs is associated with inhibition of activation of the Wnt/β-catenin pathway or non-canonical Wnt pathway-induced expression of microtubule cytoskeletal components in the developing neurons. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2139-2149, 2017. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 15493296
- Volume :
- 105
- Issue :
- 8
- Database :
- Complementary Index
- Journal :
- Journal of Biomedical Materials Research, Part A
- Publication Type :
- Academic Journal
- Accession number :
- 123804835
- Full Text :
- https://doi.org/10.1002/jbm.a.36073