Nitric oxide from brain microvascular endothelial cells may initiate the compensatory response to mild hypoxia of astrocytes in a hypoxia-inducible factor-1α dependent manner.
Year: 2016
Type: article
Abstract: ), exogenous NO blocked the degradation of HIF-1α in astrocytes but up-regulated the transcription of VEGF and LDHA, accompanied by elevated expression of VEGF protein and increased production of lactic acid. This was further confirmed by silencing of HIF-1α expression in astrocytes. In astrocytes co-cultured with primary rat BMEC under mild hypoxia, NO was released by the BMECs and prevented the degradation of HIF-1α in astrocytes, leading to the up-regulated mRNA expression of VEGF and LDHA, elevated VEGF protein expression and increased production of lactic acid. In BMECs, NO was derived from intracellular eNOS. Based on these findings, we hypothesize that, under mild hypoxia, even though astrocytes do not respond to hypoxia, NO produced by BMECs may transmit a hypoxia signal to astrocytes, triggering their adaptive response via HIF-1α.
Source: PubMed
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2603443694