Role of mitochondrial uncoupling protein 4 in rat inner ear

2011 ◽  
Vol 47 (4) ◽  
pp. 244-253 ◽  
Author(s):  
Alina Smorodchenko ◽  
Anne Rupprecht ◽  
Julia Fuchs ◽  
Johann Gross ◽  
Elena E. Pohl
Keyword(s):  
Inner Ear ◽  
Uncoupling Protein ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Uncoupling Protein 4

scholarly journals Neuroprotective Role of Mitochondrial Uncoupling Protein 2 in Cerebral Stroke

2009 ◽  
Vol 29 (6) ◽  
pp. 1069-1078 ◽  
Author(s):  
Suresh L Mehta ◽  
P. Andy Li
Keyword(s):  
Uncoupling Protein ◽  
Cellular Damage ◽  
Cerebral Stroke ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Uncoupling ◽  
Mitochondria Membrane Potential ◽  
Mitochondrial Uncoupling Protein ◽  
Mitochondrial Transporter ◽  
Develop Strategy

The uncoupling proteins (UCPs) are mitochondrial transporter proteins involved in proton conductance across inner mitochondrial membrane (IMM). UCP2, which is one of the members of this class of proteins, has a wide but restricted tissue distribution including brain. Its physiologic role according to emerging evidences, although still not clear, indicate that distribution of UCP2 may be related to regulation of mitochondria membrane potential (ΔΨm), production of reactive oxygen species (ROS), preservation of calcium homeostasis, modulation of neuronal activity, and eventually inhibition of cellular damage. These factors are very important in determining the fate of neurons and damage progression in the brain during various neurodegenerative diseases including cerebral stroke. Recent evidence indicates that an increased expression and activity of UCP2 are well correlated with neuronal survival after stroke and trauma. This review briefly covers the present understanding of UCP2, which eventually may be beneficial to understand the precise role of UCP2 to develop strategy to identify its potential therapeutic application.

scholarly journals Antioxidant and Regulatory Role of Mitochondrial Uncoupling Protein UCP2 in Pancreatic β-cells

2014 ◽  
pp. S73-S91 ◽  
Author(s):  
P. JEŽEK ◽  
T. OLEJÁR ◽  
K. SMOLKOVÁ ◽  
J. JEŽEK ◽  
A. DLASKOVÁ ◽  
...  
Keyword(s):  
Uncoupling Protein ◽  
Redox Homeostasis ◽  
Inner Mitochondrial Membrane ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Brown Adipose ◽  
Glucose Stimulated Insulin Secretion

Research on brown adipose tissue and its hallmark protein, mitochondrial uncoupling protein UCP1, has been conducted for half a century and has been traditionally studied in the Institute of Physiology (AS CR, Prague), likewise UCP2 residing in multiple tissues for the last two decades. Our group has significantly contributed to the elucidation of UCP uncoupling mechanism, fully dependent on free fatty acids (FFAs) within the inner mitochondrial membrane. Now we review UCP2 physiological roles emphasizing its roles in pancreatic β-cells, such as antioxidant role, possible tuning of redox homeostasis (consequently UCP2 participation in redox regulations), and fine regulation of glucose-stimulated insulin secretion (GSIS). For example, NADPH has been firmly established as being a modulator of GSIS and since UCP2 may influence redox homeostasis, it likely affects NADPH levels. We also point out the role of phospholipase iPLA2 isoform  in providing FFAs for the UCP2 antioxidant function. Such initiation of mild uncoupling hypothetically precedes lipotoxicity in pancreatic β-cells until it reaches the pathological threshold, after which the antioxidant role of UCP2 can be no more cell-protective, for example due to oxidative stress-accumulated mutations in mtDNA. These mechanisms, together with impaired autocrine insulin function belong to important causes of Type 2 diabetes etiology.

3,5,3′-Triiodothyronine actively stimulates UCP in brown fat under minimal sympathetic activity

1999 ◽  
Vol 276 (1) ◽  
pp. E179-E187 ◽  
Author(s):  
Marcelo Branco ◽  
Miriam Ribeiro ◽  
Nubio Negrão ◽  
Antonio C. Bianco
Keyword(s):  
Uncoupling Protein ◽  
Thermal Response ◽  
Male Rats ◽  
Intact Male ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Norepinephrine Infusion ◽  
Brown Adipose ◽  
Intact Rats

To investigate the role of type II 5′-deiodinase (5′D-II) in the expression of mitochondrial uncoupling protein (UCP) in brown adipose tissue (BAT), we injected intact male rats with reverse (r) 3,5,3′-triiodothyronine (T3; 100 μg ⋅ 100 g body wt−1 ⋅ day−1), an inhibitor of 5′D-II, for 2–5 days. UCP decreased by ∼20% in rats kept at 28°C and failed to increase during cold exposure (4°C). Next, thyroxine treatment (1–10 μg ⋅ 100 g body wt−1 ⋅ day−1) increased nuclear T3 in rats kept at 28 or 4°C. In these rats, nuclear T3 correlated positively with UCP. In addition, T3 (1–50 μg ⋅ 100 g body wt−1 ⋅ day−1) given to intact rats (5–15 days; 28°C) induced an approximately twofold increase in UCP. In these T3-treated animals, the interscapular BAT thermal response to norepinephrine infusion also correlated positively with T3 dose and UCP content. Treatment with propranolol or reserpine failed to block the T3 induction of UCP (∼1.8- and ∼2.3-fold). The results emphasize the importance of local 5′D-II and reveal an independent role of T3 in the expression of UCP.

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