Astroglia-mediated regulation of cell development in the model of neurogenic niche in vitro treated with Aβ1-42
Author(s) -
А. В. Моргун,
Е. Д. Осипова,
E. B. Boytsova,
Аnton N. Shuvaev,
Yu. K. Kоmleva,
Л. В. Труфанова,
E. F. Vais,
А. Б. Салмина
Publication year - 2019
Publication title -
biomeditsinskaya khimiya
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.192
H-Index - 15
eISSN - 2310-6972
pISSN - 2310-6905
DOI - 10.18097/pbmc20196505366
Subject(s) - neurogenesis , neuroscience , progenitor cell , neural stem cell , biology , stem cell , neurosphere , astrocyte , embryonic stem cell , progenitor , microbiology and biotechnology , hippocampal formation , cellular differentiation , adult stem cell , central nervous system , genetics , gene
Neurogenesis is a complex process which governs embryonic brain development and is importants for brain plasticity throughout the whole life. Postnatal neurogenesis occurs in neurogenic niches that regulate the processes of proliferation and differentiation of stem and progenitor cells under the action of stimuli that trigger the mechanisms of neuroplasticity. Cells of glial and endothelial origin are the key regulators of neurogenesis. It is known that physiological neurogeneses is crucial for memory formation, whereas reparative neurogenesis provides partial repair of altered brain structure and compensation of neurological deficits caused by brain injury. Dysregulation of neurogenesis is a characteristics of various neurodevelopmental and neurodegenerative diseases, particularly, Alzheimer's disease which is very important medical and social problem. In the in vitro model of the neurogenic niche using hippocampal neurospheres as a source of stem/progenitor cells and astrocytes, we studied effects of astrocyte activation on the expression of markers of different stages of cell proliferation and differentiation. We found that aberrant mechanisms of development of stem and progenitor cells, caused by the beta-amyloid (Aβ1-42), can be partially restored by targeted activation of GFAP-expressing cells in the neurogenic niche.
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