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

null Losenkova; null Zuccarini; null Helenius; Guillaume Jacquemet; null Gerasimovskaya; null Tallgren; null Jalkanen; null Yegutkin

doi:10.1016/j.bbadis.2018.03.001

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 journal › Article › Scientific › peer-review

20 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 language	Undefined/Unknown
Pages (from-to)	1804–1815
Journal	BBA - Molecular Basis of Disease
Volume	1864
Issue number	5 Pt A
DOIs	https://doi.org/10.1016/j.bbadis.2018.03.001
Publication status	Published - 2018
MoE publication type	A1 Journal article-refereed

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10.1016/j.bbadis.2018.03.001

Cite this

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

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.",

author = "Losenkova and Zuccarini and Helenius and Guillaume Jacquemet and Gerasimovskaya and Tallgren and Jalkanen and Yegutkin",

year = "2018",

doi = "10.1016/j.bbadis.2018.03.001",

language = "Odefinierat/ok{\"a}nt",

volume = "1864",

pages = "1804–1815",

journal = "BBA - Molecular Basis of Disease",

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number = "5 Pt A",

}

TY - JOUR

T1 - Endothelial cells cope with hypoxia-induced depletion of ATP via activation of cellular purine turnover and phosphotransfer networks.

AU - Losenkova, null

AU - Zuccarini, null

AU - Helenius, null

AU - Jacquemet, Guillaume

AU - Gerasimovskaya, null

AU - Tallgren, null

AU - Jalkanen, null

AU - Yegutkin, null

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

U2 - 10.1016/j.bbadis.2018.03.001

DO - 10.1016/j.bbadis.2018.03.001

M3 - Artikel

SN - 0925-4439

VL - 1864

SP - 1804

EP - 1815

JO - BBA - Molecular Basis of Disease

JF - BBA - Molecular Basis of Disease

IS - 5 Pt A

ER -