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Comparative analysis of transcriptomes from the carotid body, adrenal medulla, and superior cervical ganglion of adult mice

ABSTRACT: Acute O2 sensing is a fundamental property of cells in the peripheral chemoreceptors, e.g. glomus cells in the carotid body (CB) and chromaffin cells in the adrenal medulla (AM), and is necessary for adaptation to hypoxia. The mechanisms underlying the detection of changes in O2 tension by these cells are still poorly understood. Recently, we suggested that CB glomus cells have specific metabolic features that favour their sensitivity to hypoxia (Fernandez-Aguera et al, 2015, Cell Metab.). To investigate the metabolic profile characteristic of acute O2-sensing cells, we used adult mice to compare the transcriptomes of three organs derived from common sympathoadrenal progenitors, but exhibiting variable responsiveness to acute hypoxia: CB and AM which are O2-sensitive (CB > AM) and superior cervical ganglion (SCG), which are practically O2-insensitive. Our data support the concept that responsiveness to acute hypoxia depends on a “signature metabolic profile” in peripheral chemoreceptor cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE99593 | GEO | 2017/09/08

SECONDARY ACCESSION(S): PRJNA388928

REPOSITORIES: GEO

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Project description:Oxygen fluctuation during tissue remodeling imposes a major metabolic challenge in human tumors. Stem-like tumor cells in glioblastomas are believed to possess extraordinary metabolic flexibility, enabling them to initiate growth even under non-permissive conditions. To identify adaptive response mechanism, we compared the effects of acute and chronic hypoxia versus oxygenation on stem-like glioblastoma (GS) cells. GS cell lines were established and propagated either under normoxia (21% O2) or hypoxia (1% O2) and subsequently exposed to acute normoxia or hypoxia, respectively. Gene expression profiling revealed that acute hypoxia predominantly induced metabolic pathways and cell cycle arrest, whereas chronic hypoxia activated neurodevelopmental processes. In particular, we found increased expression of glycolytic enzymes, especially of the preparatory phase of glycolysis, under acute hypoxia, whereas pentose phosphate pathway (PPP) enzymes were downregulated. The opposite was found for acute oxygenation of hypoxic GS cells. Findings were confirmed by qPCR and immunoblot analyses. Despite downregulation by hypoxia, expression of PPP enzymes is increased in GBMs compared to normal brain, whereas expression of hypoxia-inducible enzymes of the parallel preparatory phase of glycolysis is decreased. Immunohistochemistry revealed strong staining for PPP enzymes in the bulk of GBM tissue, especially in highly proliferative areas, but not in pseudopalisading (hypoxic) cells. Glycolytic enzymes displayed an inverse pattern. Mass spectrometric analysis using [1,2-13C2]-D-glucose showed reduced glucose flux through the PPP under hypoxia in favor of flux through glycolysis. Acute and chronic hypoxia increased cell migration but reduced proliferation, whereas normoxia had opposite effects. Our findings extend Warburg’s observations by showing that in most tumor cells the PPP, which supplies metabolites for biomass production, is favored over the parallel preparatory phase of glycolysis, but is suppressed under acute severe hypoxia, causing a switch to direct glycolysis to protect against hypoxic stress.

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Comparative analysis of transcriptomes from the carotid body, adrenal medulla, and superior cervical ganglion of adult mice

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