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P-hydroxy benzaldehyde facilitates reprogramming of reactive astrocytes into neurons via endogenous transcriptional regulation.
- Source :
- International Journal of Neuroscience; Oct2023, Vol. 133 Issue 10, p1096-1108, 13p
- Publication Year :
- 2023
-
Abstract
- Cerebral ischemia leads to linguistic and motor dysfunction, as the death of neurons in ischemic core is permanent and non-renewable. An innovative avenue is to induce and/or facilitate reprogramming of adjacent astrocytes into neurons to replace the lost neurons and re-establish brain homeostasis. This study aimed to investigate whether the p-hydroxy benzaldehyde (p-HBA), a phenolic compound isolated from Gastrodia elata Blume, could facilitate the reprogramming of oxygen-glucose deprivation/reperfusion (OGD/R)-damaged astrocytes into neurons. The primary parenchymal astrocytes of rat were exposure to OGD and reperfusion with define culture medium. Cells were then incubated with different concentration of p-HBA (1, 10, 100, 400 μM) and collected at desired time point for reprogramming process analysis. OGD/R could elicit endogenous neurogenic program in primary parenchymal astrocytes of rat under define culture condition, and these so-called reactive astrocytes could be reprogrammed into neurons. However, the neonatal neurons produced by this endogenous procedure could not develop into mature neurons, and the conversion rate was only 1.9%. Treatment of these reactive astrocytes with p-HBA could successfully promote the conversion rate to 6.1%, and the neonatal neurons could develop into mature neurons within 14 days. Further analysis showed that p-HBA down-regulated the Notch signal component genes Dll1, Hes1 and SOX2, while the transcription factor NeuroD1 was up-regulated. The results of this study demonstrated that p-HBA facilitated the astrocyte-to-neuron conversion. This chemical reprogramming was mediated by inhibition of Notch1 signaling pathway and transcriptional activation of NeuroD1. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00207454
- Volume :
- 133
- Issue :
- 10
- Database :
- Complementary Index
- Journal :
- International Journal of Neuroscience
- Publication Type :
- Academic Journal
- Accession number :
- 172441658
- Full Text :
- https://doi.org/10.1080/00207454.2022.2049775