Double-Edged Sword of Vitamin D3 Effects on Primary Neuronal Cultures in Hypoxic States
Autor: | Maria Vedunova, Mikhail Krivonosov, Svetlana Guseva, Maria S. Gavrish, Tatiana A. Mishchenko, Mikhail Ivanchenko, Julia Fedotova, Maria O. Savyuk, Maria M. Loginova |
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Rok vydání: | 2021 |
Předmět: |
Vitamin
vitamin D3 cholecalciferol functional neural network activity QH301-705.5 Cell Survival primary neuronal cultures chemistry.chemical_element Tropomyosin receptor kinase B Pharmacology Calcium Neuroprotection Catalysis Article Inorganic Chemistry chemistry.chemical_compound medicine Animals Receptor trkB Viability assay Physical and Theoretical Chemistry Biology (General) Molecular Biology Transcription factor QD1-999 Spectroscopy Cells Cultured Neurons hypoxia Brain-Derived Neurotrophic Factor Organic Chemistry General Medicine Hypoxia (medical) Hypoxia-Inducible Factor 1 alpha Subunit Computer Science Applications Mice Inbred C57BL Chemistry Neuroprotective Agents chemistry medicine.symptom Cholecalciferol Neuroglia |
Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 22, Iss 5417, p 5417 (2021) Volume 22 Issue 11 |
ISSN: | 1422-0067 |
Popis: | The use of vitamin D3 along with traditional therapy opens up new prospects for increasing the adaptive capacity of nerve cells to the effects of a wide range of stress factors, including hypoxia-ischemic processes. However, questions about prophylactic and therapeutic doses of vitamin D3 remain controversial. The purpose of our study was to analyze the effects of vitamin D3 at different concentrations on morpho-functional characteristics of neuron–glial networks in hypoxia modeling in vitro. We showed that a single administration of vitamin D3 at a high concentration (1 µM) in a normal state has no significant effect on the cell viability of primary neuronal cultures however, it has a pronounced modulatory effect on the functional calcium activity of neuron–glial networks and causes destruction of the network response. Under hypoxia, the use of vitamin D3 (1 µM) leads to total cell death of primary neuronal cultures and complete negation of functional neural network activity. In contrast, application of lower concentrations of vitamin D3 (0.01 µM and 0.1 µM) caused a pronounced dose-dependent neuroprotective effect during the studied post-hypoxic period. While the use of vitamin D3 at a concentration of 0.1 µM maintained cell viability, preventive administration of 0.01 µM not only partially preserved the morphological integrity of primary neuronal cells but also maintained the functional structure and activity of neuron–glial networks in cultures. Possible molecular mechanisms of neuroprotective action of vitamin D3 can be associated with the increased expression level of transcription factor HIF-1α and maintaining the relationship between the levels of BDNF and TrkB expression in cells of primary neuronal cultures. |
Databáze: | OpenAIRE |
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