Literature DB >> 31694441

The selective BDNF overexpression in neurons protects neuroglial networks against OGD and glutamate-induced excitotoxicity.

S G Gaidin1, M V Turovskaya1, M S Gavrish2, A A Babaev2, V N Mal'tseva1, E V Blinova3,4, E A Turovsky1.   

Abstract

Objective: Cerebral ischemia is accompanied by damage and death of a significant number of neurons due to glutamate excitotoxicity with subsequent a global increase of cytosolic Ca2+ concentration ([Ca2+]i). This study aimed to investigate the neuroprotective action of BDNF overexpression in hippocampal neurons against injury under ischemia-like conditions (oxygen and glucose deprivation) and glutamate-induced excitotoxicity (GluTox).
Methods: The overexpression of BDNF was reached by the transduction of cell cultures with the adeno-associated (AAV)-Syn-BDNF-EGFP virus construct. Neuroprotective effects were mediated by Ca2+-dependent BDNF release followed by activation of the neuroprotective signaling cascades and changes of the gene expression. Thus, BDNF overexpression modulates Ca2+ homeostasis in cells, preventing Ca2+ overload and initiation of apoptotic and necrotic processes.
Results: Antiapoptotic effect of BDNF overexpression is mediated via activation of phosphoinositide-3-kinase (PI3K) pathway and changing the expression of PI3K, HIF-1, Src and an anti-inflammatory cytokine IL-10. On the contrary, the decrease of expression of proapoptotic proteins such as Jun, Mapk8, caspase-3 and an inflammatory cytokine IL-1β was observed. These changes of expression were accompanied by the decrease of quantity of IL-1β receptors and the level of TNFα in cells in control, as well as 24 h after OGD. Besides, BDNF overexpression changes the expression of GABA(B) receptors. Also, the expression of NMDA and AMPA receptor subunits was altered towards a change in the conductivity of the receptors for Ca2+.
Conclusion: Thus, our results demonstrate that neuronal BDNF overexpression reveals complex neuroprotective effects on the neurons and astrocytes under OGD and GluTox via inhibition of Ca2+ responses and regulation of gene expression.

Entities:  

Keywords:  BDNF; Ischemia; apoptosis; astrocytes; calcium; cell death; glutamate excitotoxicity; neurons; neuroprotection; receptors; signal transduction

Mesh:

Substances:

Year:  2019        PMID: 31694441     DOI: 10.1080/00207454.2019.1691205

Source DB:  PubMed          Journal:  Int J Neurosci        ISSN: 0020-7454            Impact factor:   2.292


  13 in total

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