CoCl₂-Mimicked Endothelial Cell Hypoxia Induces Nucleotide Depletion and Functional Impairment That Is Reversed by Nucleotide Precursors.

ABSTRACT: Chronic hypoxia drives vascular dysfunction by various mechanisms, including changes in mitochondrial respiration. Although endothelial cells (ECs) rely predominantly on glycolysis, hypoxia is known to alter oxidative phosphorylation, promote oxidative stress and induce dysfunction in ECs. Our work aimed to analyze the effects of prolonged treatment with hypoxia-mimetic agent CoCl₂ on intracellular nucleotide concentration, extracellular nucleotide breakdown, mitochondrial function, and nitric oxide (NO) production in microvascular ECs. Moreover, we investigated how nucleotide precursor supplementation and adenosine deaminase inhibition protected against CoCl₂-mediated disturbances. Mouse (H5V) and human (HMEC-1) microvascular ECs were exposed to CoCl₂-mimi

SUBMITTER: Kutryb-Zajac B 

PROVIDER: S-EPMC9313011 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature