ArticleBiochimica et biophysica acta2013
Glycolysis-respiration relationships in a neuroblastoma cell line.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
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- Metabolic protein kinase signalling in neuroblastoma.Molecular metabolism · 2023Review
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- High-Resolution Respirometry in Assessment of Mitochondrial Function in Neuroblastoma SH-SY5Y Intact Cells.The Journal of membrane biology · 2020Article
- Mitochondrial Respiration inCancers · 2020Article
- Mitochondrial DNA Manipulations Affect Tau Oligomerization.Journal of Alzheimer's disease : JAD · 2020Article
- Conserved roles of glucose in suppressing reactive oxygen species-induced cell death and animal survival.Aging · 2019Article
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- Strategies to detect mitochondrial oxidants.Redox biology · 2019Review
- Pharmacologic ascorbate induces neuroblastoma cell death by hydrogen peroxide mediated DNA damage and reduction in cancer cell glycolysis.Free radical biology & medicine · 2017Article
- Selective elimination of neuroblastoma cells by synergistic effect of Akt kinase inhibitor and tetrathiomolybdate.Journal of cellular and molecular medicine · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough some reciprocal glycolysis-respiration relationships are well recognized, the relationship between reduced glycolysis flux and mitochondrial respiration has not been critically characterized.
methodsWe concomitantly measured the extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) of SH-SY5Y neuroblastoma cells under free and restricted glycolysis flux conditions.
resultsUnder conditions of fixed energy demand ECAR and OCR values showed a reciprocal relationship. In addition to observing an expected Crabtree effect in which increasing glucose availability raised the ECAR and reduced the OCR, a novel reciprocal relationship was documented in which reducing the ECAR via glucose deprivation or glycolysis inhibition increased the OCR. Substituting galactose for glucose, which reduces net glycolysis ATP yield without blocking glycolysis flux, similarly reduced the ECAR and increased the OCR. We further determined how reduced ECAR conditions affect proteins that associate with energy sensing and energy response pathways. ERK phosphorylation, SIRT1, and HIF1a decreased while AKT, p38, and AMPK phosphorylation increased.
conclusionsThese data document a novel intracellular glycolysis-respiration effect in which restricting glycolysis flux increases mitochondrial respiration. GENERAL SIGNIFICANCE: Since this effect can be used to manipulate cell bioenergetic infrastructures, this particular glycolysis-respiration effect can practically inform the development of new mitochondrial medicine approaches.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.