Hyperoxia induces glutamine-fuelled anaplerosis in retinal Müller cells

Charandeep Singh, Vincent Tran, Leah McCollum, Youstina Bolok, Kristin Allan, Alex Yuan, George Hoppe, Henri Brunengraber and Jonathan E. Sears ()
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Charandeep Singh: Cole Eye Institute, Cleveland Clinic
Vincent Tran: Cole Eye Institute, Cleveland Clinic
Leah McCollum: Cole Eye Institute, Cleveland Clinic
Youstina Bolok: Cole Eye Institute, Cleveland Clinic
Kristin Allan: Cole Eye Institute, Cleveland Clinic
Alex Yuan: Cole Eye Institute, Cleveland Clinic
George Hoppe: Cole Eye Institute, Cleveland Clinic
Henri Brunengraber: Case Western Reserve School of Medicine Cleveland
Jonathan E. Sears: Cole Eye Institute, Cleveland Clinic

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract Although supplemental oxygen is required to promote survival of severely premature infants, hyperoxia is simultaneously harmful to premature developing tissues such as in the retina. Here we report the effect of hyperoxia on central carbon metabolism in primary mouse Müller glial cells and a human Müller glia cell line (M10-M1 cells). We found decreased flux from glycolysis entering the tricarboxylic acid cycle in Müller cells accompanied by increased glutamine consumption in response to hyperoxia. In hyperoxia, anaplerotic catabolism of glutamine by Müller cells increased ammonium release two-fold. Hyperoxia induces glutamine-fueled anaplerosis that reverses basal Müller cell metabolism from production to consumption of glutamine.

Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-15066-6

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DOI: 10.1038/s41467-020-15066-6

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