Endothelial cells cope with hypoxia-induced depletion of ATP via activation of cellular purine turnover and phosphotransfer networks.

Losenkova, Zuccarini, Helenius, Guillaume Jacquemet, Gerasimovskaya, Tallgren, Jalkanen, Yegutkin

Research output: Contribution to journalArticleScientificpeer-review

10 Citations (Scopus)

Abstract

H]ADP/ATP. Furthermore, following a period of hypoxia, HUVEC underwent concurrent changes in intracellular signaling manifested in the depletion of putative ATP stores and targeted up-regulation of phospho-p53, p70S6K/mTOR and other tyrosine kinases. The revealed complex implication of both extrinsic and intrinsic mechanisms into a tuned hypoxia-induced control of purine homeostasis and signaling may open up further research for the development of pharmacological treatments to improve endothelial cell function under disease conditions associated with a loss of cellular ATP during oxygen deprivation.
Original languageUndefined/Unknown
Pages (from-to)1804–1815
JournalBBA - Molecular Basis of Disease
Volume1864
Issue number5 Pt A
DOIs
Publication statusPublished - 2018
MoE publication typeA1 Journal article-refereed

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