Novel Functions Of Stanniocalcin-1(STC1) Through Uncoupling Protein 2 (UCP2) Up-Regulation; Promoting Survival Of Cancer Cells Under Oxidative Stress And Inducing The Uncoupling Respiration (Warburg Effect)

2012 ◽  
Author(s):  
Shinya Ohkouchi ◽  
Masahiko Kanehira ◽  
Toshiaki Kikuchi ◽  
Masahito Ebina
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Warburg Effect ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2

scholarly journals The Warburg Effect in Leukemia-Stroma Cocultures Is Mediated by Mitochondrial Uncoupling Associated with Uncoupling Protein 2 Activation

2008 ◽  
Vol 68 (13) ◽  
pp. 5198-5205 ◽  
Author(s):  
Ismael Samudio ◽  
Michael Fiegl ◽  
Teresa McQueen ◽  
Karen Clise-Dwyer ◽  
Michael Andreeff
Keyword(s):  
Warburg Effect ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Mitochondrial Uncoupling ◽  
The Warburg Effect

Ablation of uncoupling protein 2 exacerbates salt-induced cardiovascular and renal remodeling associated with enhanced oxidative stress

2014 ◽  
Vol 175 (1) ◽  
pp. 206-210 ◽  
Author(s):  
Shuangtao Ma ◽  
Yan Zhang ◽  
Qiang Wang ◽  
Dachun Yang ◽  
De Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2

scholarly journals Genipin-Induced Inhibition of Uncoupling Protein-2 Sensitizes Drug-Resistant Cancer Cells to Cytotoxic Agents

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13289 ◽  
Author(s):  
Ryan J. Mailloux ◽  
Cyril Nii-Klu Adjeitey ◽  
Mary-Ellen Harper
Keyword(s):  
Cancer Cells ◽  
Uncoupling Protein ◽  
Cytotoxic Agents ◽  
Uncoupling Protein 2 ◽  
Drug Resistant

Low-level lasers on microRNA and uncoupling protein 2 mRNA levels in human breast cancer cells

Laser Physics ◽  
2017 ◽  
Vol 27 (6) ◽  
pp. 065601 ◽  
Author(s):  
K S Canuto ◽  
A F Teixeira ◽  
J A Rodrigues ◽  
F Paoli ◽  
E M Nogueira ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Mrna Levels ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Low Level

Increased reactive oxygen species production with antisense oligonucleotides directed against uncoupling protein 2 in murine endothelial cells

2002 ◽  
Vol 80 (6) ◽  
pp. 757-764 ◽  
Author(s):  
Carine Duval ◽  
Anne Nègre-Salvayre ◽  
Alain Doglio ◽  
Robert Salvayre ◽  
Luc Pénicaud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Antisense Oligonucleotides ◽  
Uncoupling Protein ◽  
Reactive Oxygen ◽  
Ldl Oxidation ◽  
Uncoupling Protein 2 ◽  
Thiobarbituric Acid Reactive Substance ◽  
Oxygen Species

Uncoupling protein 2 (UCP-2) belongs to the mitochondrial anion carrier family. It is ubiquitously expressed but is most abdundant in the reticuloendothelial system. In addition to uncoupling function, UCP-2 modulates the production of reactive oxygen species (ROS) by isolated mitochondria. Using an antisense oligonucleotide strategy, we investigated whether a defect in UCP-2 expression modulates ROS in intact endothelial cells. Murine endothelial cells (CRL 2181) pretreated by antisense oligonucleotides directed against UCP-2 mRNA exhibited a significant and specific increase in membrane potential and intracellular ROS level compared with control scrambled or anti-UCP-1 and -UCP-3 antisense oligonucleotides. These specific changes induced by UCP-2 antisense oligonucleotides were correlated with a rise in extracellular superoxide anion production and oxidative stress assessed by thiobarbituric acid reactive substance values. Taken together, these data suggest a role for UCP-2 in control of ROS production and subsequent oxidation of surrounding compounds mediating oxidative stress of endothelial cells. These data also support the notion that manipulations of UCP-2 at the genetic level could control ROS metabolism at the cellular level.Key words: UCP-2, reactive oxygen species, LDL oxidation, oxidative stress, mitochondria, endothelial cells.

215. Placental expression of uncoupling protein-2 is reduced by glucocorticoid treatment in late pregnancy: implications for placental oxidative stress

2008 ◽  
Vol 20 (9) ◽  
pp. 15
Author(s):  
M. L. Jones ◽  
P. J. Mark ◽  
B. J. Waddell
Keyword(s):  
Oxidative Stress ◽  
Gestational Age ◽  
Uncoupling Protein ◽  
Late Pregnancy ◽  
Uncoupling Protein 2 ◽  
Dexamethasone Treatment ◽  
Glucocorticoid Treatment ◽  
Ucp2 Expression ◽  
Endogenous Protection ◽  
Placental Oxidative Stress

Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders in humans, most notably in preeclampsia (PE) and intrauterine growth restriction (IUGR). Protection from oxidative stress is provided by antioxidant enzymes including superoxide dismutase-1 and 2 (SOD-1 and –2) and catalase (CAT), which convert reactive oxygen species (ROS) to inert products. It has also been proposed that uncoupling protein-2 (UCP2) may limit oxidative stress by reducing ROS production, but little is known of UCP2 expression in placenta. Here we measured placental UCP2, SOD-1, SOD-2 and CAT mRNA expression (by qRT–PCR) in normal gestation and after glucocorticoid-induced IUGR. The latter was included because glucocorticoids can increase oxidative stress in other tissues, and placental glucocorticoid exposure is elevated in both PE and IUGR. Placentas were collected on days 16 and 22 of normal pregnancy (term = day 23) and on day 22 after dexamethasone treatment (0.75 mg/mL in drinking water from day 13). The two morphologically-distinct regions of the placenta, the junctional (JZ) and labyrinth (LZ) zones, were analysed separately because effectively all growth occurs in the LZ over this period. Expression of UCP2 in LZ exceeded that in JZ (P < 0.001) and increased in both zones between days 16 and 22 (LZ: 2.0-fold; JZ: 3.2-fold). Dexamethasone treatment reduced UCP2 in LZ (44%; P < 0.05) but not in JZ. SOD1 and SOD2 increased with gestational age in LZ (P < 0.01) and JZ (P < 0.05), but neither were affected by dexamethasone. CAT expression was higher (2.4-fold, P < 0.001) in LZ compared with JZ but did not change with gestational age or dexamethasone. In summary, these data suggest that endogenous protection against oxidative stress increases in the rat placenta during late pregnancy. Moreover, this protection may be compromised by reduced placental UCP2 expression in a model of glucocorticoid-induced IUGR.

Lopimune-induced mitochondrial toxicity is attenuated by increased uncoupling protein-2 level in treated mouse hepatocytes

2015 ◽  
Vol 468 (3) ◽  
pp. 401-407 ◽  
Author(s):  
Sara El Hoss ◽  
Georges M. Bahr ◽  
Karim S. Echtay
Keyword(s):  
Oxidative Stress ◽  
Protease Inhibitor ◽  
Regulatory Mechanism ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Ros Production ◽  
Mitochondrial Toxicity ◽  
Mouse Hepatocytes ◽  
Proton Leakage ◽  
Feedback Regulatory Mechanism

We have demonstrated that the antiretroviral protease inhibitor Lopimune increases oxidative stress in mouse hepatocytes and subsequently mitochondrial proton leakage. This effect is mediated by increased uncoupling protein-2 expression which in turn inhibits ROS production as a negative feedback regulatory mechanism.

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