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

A1 Originalartikel i en vetenskaplig tidskrift (referentgranskad)

Interna författare/redaktörer

Publikationens författare: Losenkova, Zuccarini, Helenius, Jacquemet, Gerasimovskaya, Tallgren, Jalkanen, Yegutkin
Publiceringsår: 2018
Tidskrift: BBA - Molecular Basis of Disease
Tidskriftsakronym: Biochim Biophys Acta Mol Basis Dis
Volym: 1864
Nummer: 5 Pt A
Artikelns första sida, sidnummer: 1804
Artikelns sista sida, sidnummer: 1815
ISSN: 0925-4439


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.

Senast uppdaterad 2019-14-11 vid 03:51