scholarly journals Activation and Function of Mitochondrial Uncoupling Protein in Plants

2004 ◽  
Vol 279 (50) ◽  
pp. 51944-51952 ◽  
Author(s):  
Anna M. O. Smith ◽  
R. George Ratcliffe ◽  
Lee J. Sweetlove
Keyword(s):  
Transgenic Plants ◽  
Protein Content ◽  
Uncoupling Protein ◽  
Tricarboxylic Acid Cycle ◽  
Proton Conductance ◽  
Mitochondrial Uncoupling ◽  
Experimental Conditions ◽  
Mitochondrial Uncoupling Protein ◽  
Exact Function

Plant mitochondrial uncoupling protein (UCP) is activated by superoxide suggesting that it may function to minimize mitochondrial reactive oxygen species (ROS) formation. However, the precise mechanism of superoxide activation and the exact function of UCP in plants are not known. We demonstrate that 4-hydroxy-2-nonenal (HNE), a product of lipid peroxidation, and a structurally related compound,trans-retinal, stimulate a proton conductance in potato mitochondria that is inhibitable by GTP (a characteristic of UCP). Proof that the effects of HNE andtrans-retinal are mediated by UCP is provided by examination of proton conductance in transgenic plants overexpressing UCP. These experiments demonstrate that the mechanism of activation of UCP is conserved between animals and plants and imply a conservation of function. Mitochondria from transgenic plants overexpressing UCP were further studied to provide insight into function. Experimental conditions were designed to mimic a bioenergetic state that might be foundin vivo(mitochondria were supplied with pyruvate as well as tricarboxylic cycle acids atin vivocytosolic concentrations and an exogenous ATP sink was established). Under such conditions, an increase in UCP protein content resulted in a modest but significant decrease in the rate of superoxide production. In addition,13C-labeling experiments revealed an increase in the conversion of pyruvate to citrate as a result of increased UCP protein content. These results demonstrate that under simulatedin vivoconditions, UCP is active and suggest that UCP may influence not only mitochondrial ROS production but also tricarboxylic acid cycle flux.

Thermoregulatory responses of the inbred heat-tolerant FOK rat to cold

1999 ◽  
Vol 277 (2) ◽  
pp. R362-R367 ◽  
Author(s):  
Takehiro Yahata ◽  
Fujiya Furuyama ◽  
Tomoaki Nagashima ◽  
Mitsuru Moriya ◽  
Kazue Kikuchi-Utsumi ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Uncoupling Protein ◽  
High Capacity ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Brown Adipose ◽  
Heat Tolerant ◽  
Colonic Temperature

The responses of inbred heat-tolerant FOK rats to cold were compared with those of Wistar King A/H (WKAH) and Std:Wistar (WSTR) strains. The fall of colonic temperature during cold exposure was unexpectedly smaller in FOK than in other groups, but the onset of shivering was delayed in FOK. Norepinephrine (NE)-induced in vivo oxygen consumption and the mitochondrial uncoupling protein 1 level of brown adipose tissue (BAT) were not different among the groups, but the cold-induced increases in in vivo oxygen consumption as well as plasma glycerol and free fatty acids were higher in FOK than in other groups. In vitro NE-induced oxygen consumption of BAT was less in FOK than WSTR, but not WKAH. The magnitude of the NE-induced increase in blood flow through BAT was higher in FOK than in other groups. These results suggest that FOK paradoxically have a high capacity for nonshivering thermogenesis in spite of their high capacity for heat tolerance, probably due to an increased lipid utilization and improved circulation of BAT.

scholarly journals Thermogenesis in newborn rats after prenatal or postnatal hypoxia

1998 ◽  
Vol 85 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Jacopo P. Mortola ◽  
Lina Naso
Keyword(s):  
Chronic Hypoxia ◽  
Uncoupling Protein ◽  
Perinatal Period ◽  
Mitochondrial Uncoupling ◽  
Experimental Conditions ◽  
Interscapular Brown Adipose Tissue ◽  
Mitochondrial Uncoupling Protein ◽  
Brown Adipose ◽  
Old Rats ◽  
Thermogenic Capacity

Oxygen consumption (V˙o 2) was measured in normoxia as ambient temperature (Ta) was lowered from 40 to 15°C, at the rate of 0.5°C/min (thermoneutrality ∼33°C). In 2-day-old rats born in hypoxia after hypoxic gestation, the Ta-V˙o 2relationship was as in controls; their interscapular brown adipose tissue (IBAT) was hypoplastic (less proteins and DNA), with lower concentration of the mitochondrial uncoupling protein thermogenin. In 8-day-old rats exposed to hypoxia postnatally ( day 2 to day 8), at any Ta below thermoneutralityV˙o 2 was higher than in controls; also, in this group IBAT was hypoplastic with decreased thermogenin. Additional measurements under various experimental conditions indicated that the increased thermogenic capacity was not explained by the smaller body mass and increased blood oxygen content or by the eventuality of intermittent cold stimuli during the chronic hypoxia. On the other hand, chronic hypercapnia (3% CO2 in normoxia, from day 2 to day 8) also resulted in increased normoxic thermogenesis. We conclude that chronic hypoxia in the perinatal period 1) reduces IBAT mass and thermogenin concentration and 2) can increase the newborn’s thermogenic capacity because of stress-related mechanisms not specific to hypoxia.

scholarly journals Effects of Mitochondrial Uncoupling Protein 2 Inhibition by Genipin in Human Cumulus Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Hongshan Ge ◽  
Fan Zhang ◽  
Dan Shan ◽  
Hua Chen ◽  
Xiaona Wang ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Uncoupling Protein ◽  
Physiological Role ◽  
Cumulus Cells ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Cultural Medium ◽  
Cellular Autophagy ◽  
Significant Difference ◽  
Active Caspase

UCP2 plays a physiological role by regulating mitochondrial biogenesis, maintaining energy balance, ROS elimination, and regulating cellular autophagy in numerous tissues. But the exact roles of UCP2 in cumulus cells are still not clear. Genipin, a special UCP2 inhibitor, was added into the cultural medium to explore the roles of UCP2 in human cumulus cells. There were no significant differences in ATP and mitochondrial membrane potential levels in cumulus cells from UCP2 inhibiting groups as compared with the control. The levels of ROS and Mn-SOD were markedly elevated after UCP2 inhibited Genipin. However, the ratio of reduced GSH to GSSG significantly declined after treatment with Genipin. UCP2 inhibition by Genipin also resulted in obvious increase in the active caspase-3, which accompanied the decline of caspase-3 mRNA. The level of progesterone in culture medium declined obviously after Genipin treatment. But there was no significant difference in estradiol concentrations. This study indicated that UCP2 is expressed in human cumulus cells and plays important roles on mediate ROS production, apoptotic process, and steroidogenesis, suggesting UCP2 may be involved in regulation of follicle development and oocyte maturation and quality.

scholarly journals Mitochondrial Hormesis in PancreaticβCells: Does Uncoupling Protein 2 Play a Role?

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Ning Li ◽  
Suzana Stojanovski ◽  
Pierre Maechler
Keyword(s):  
Stress Responses ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Cell Function ◽  
Uncoupling Protein ◽  
Glucose Sensing ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Cellular Stresses ◽  
Excessive Nutrients

In pancreaticβcells, mitochondrial metabolism translates glucose sensing into signals regulating insulin secretion. Chronic exposure ofβcells to excessive nutrients, namely, glucolipotoxicity, impairsβ-cell function. This is associated with elevated ROS production from overstimulated mitochondria. Mitochondria are not only the major source of cellular ROS, they are also the primary target of ROS attacks. The mitochondrial uncoupling protein UCP2, even though its uncoupling properties are debated, has been associated with protective functions against ROS toxicity. Hormesis, an adaptive response to cellular stresses, might contribute to the protection againstβ-cell death, possibly limiting the development of type 2 diabetes. Mitochondrial hormesis, or mitohormesis, is a defense mechanism observed in ROS-induced stress-responses by mitochondria. Inβcells, mitochondrial damages induced by sublethal exogenous H2O2can induce secondary repair and defense mechanisms. In this context, UCP2 is a marker of mitohormesis, being upregulated following stress conditions. When overexpressed in nonstressed naïve cells, UCP2 confers resistance to oxidative stress. Whether treatment with mitohormetic inducers is sufficient to restore or ameliorate secretory function ofβcells remains to be determined.

scholarly journals Mitochondrial uncoupling protein 2 (UCP2), but not UCP3, is sensitive to oxygen concentration in cells

2020 ◽  
Author(s):  
Karolina E. Hilse ◽  
Anne Rupprecht ◽  
Kristopher Ford ◽  
Olena Andrukhova ◽  
Reinhold Erben ◽  
...  
Keyword(s):  
Stem Cell ◽  
Oxygen Concentration ◽  
Uncoupling Protein ◽  
Ischemia Reperfusion ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation ◽  
Mitochondrial Uncoupling ◽  
Homologous Proteins ◽  
Mitochondrial Uncoupling Protein ◽  
Pathological Conditions

AbstractOne of the important hallmarks of cardiovascular disease is mitochondrial dysfunction, which results in abnormal energy metabolism and increased ROS production in cardiomyocytes. Members of the mitochondrial uncoupling protein family, UCP2 and UCP3, are thought to be beneficial by reducing ROS due to mild uncoupling. More recent hypotheses suggest the involvement of both proteins in cell metabolism by the transport of yet unknown substrates. The protein expression pattern under physiological and pathological conditions is an important clue for the evaluation of UCP2/UCP3 function, however, there is still no consensus about it. Previously, we demonstrated that only UCP3 is present in the adult murine heart under physiological conditions and correlated it with the predominant use of fatty acids for oxidation. In contrast, UCP2 was found only in very young (stem cell – like) cardiomyocytes, that rely mostly on glycolysis. Here, we employed three different models (ex vivo heart ischemia-reperfusion model, myocardial infarction model, and embryonic stem cell differentiation into cardiomyocytes under hypoxic conditions) to evaluate the abundance of both proteins under ischemia and hypoxia conditions. We found that (i) oxygen shortage or bursts did not influence UCP3 levels in the heart and ii) UCP2 was not present in healthy, ischemic, or re-perfused hearts. However, (iii) UCP2 was sensitive to the oxygen concentration in stem cells, in which UCP2 is normally expressed. These results further support the idea, that two highly homologous proteins – UCP2 and UCP3 – are abundant in different cells and tissues, and differently regulated under physiological and pathological conditions.

scholarly journals Mitochondrial Uncoupling protein‐2 regulates NLRP3 inflammasome

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Rajan babu Venugopal ◽  
Ruan Rollin Cox ◽  
prasanna Tamarappu Parthasarathy ◽  
Richard F Lockey ◽  
Narasaiah Kolliputi
Keyword(s):  
Nlrp3 Inflammasome ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein
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