Uncoupling protein 2 modulates cell viability in adult rat cardiomyocytes

2007 ◽  
Vol 293 (1) ◽  
pp. H829-H835 ◽  
Author(s):  
Natalya Bodyak ◽  
Debra L. Rigor ◽  
Yee-Shiuan Chen ◽  
Yuchi Han ◽  
Egbert Bisping ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Myocytes ◽  
Rat Heart ◽  
Uncoupling Protein ◽  
Atp Depletion ◽  
Uncoupling Protein 2 ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Rat Cardiac Myocytes ◽  
Hypoxia Reoxygenation

Uncoupling protein 2 (UCP2) is an inner mitochondrial membrane proton carrier that uncouples ATP synthesis. The aim of this study was to determine whether UCP2 plays a role in survival of adult rat cardiac myocytes. We first studied the effects of UCP2 overexpression in vitro. Overexpression of UCP2 in primary cardiomyocytes led to a significant decline in ATP level and the development of acidosis but had no observable effect on cell survival. When cardiomyocytes were challenged with hypoxia-reoxygenation, cells overexpressing UCP2 survived significantly less compared with control. This finding was associated with upregulation of proapoptotic protein Bcl-2 and 19-kDa interacting protein 3 (BNIP3). Furthermore, UCP2 short interfering RNA prevented both the increase in cell death and BNIP3 expression. To examine the in vivo role of UCP2 in the heart, we used the Dahl salt-sensitive rat heart-failure model. Northern blot analysis revealed that UCP2 mRNA level was significantly upregulated in rat heart failure along with BNIP3 protein level. In conclusion, UCP2 increases sensitivity of adult rat cardiac myocytes to hypoxia-reoxygenation by way of ATP depletion and acidosis, which in turn causes accumulation of prodeath protein BNIP3.

scholarly journals Mitochondrial uncoupling protein-2 deficiency protects steatotic mouse hepatocytes from hypoxia/reoxygenation

2012 ◽  
Vol 302 (3) ◽  
pp. G336-G342 ◽  
Author(s):  
Zachary P. Evans ◽  
Arun P. Palanisamy ◽  
Alton G. Sutter ◽  
Justin D. Ellett ◽  
Venkat K. Ramshesh ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Uncoupling Protein ◽  
Thiobarbituric Acid ◽  
Atp Depletion ◽  
Uncoupling Protein 2 ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Ucp2 Expression ◽  
Hypoxia Reoxygenation

Steatotic livers are sensitive to ischemic events and associated ATP depletion. Hepatocellular necrosis following these events may result from mitochondrial uncoupling protein-2 (UCP2) expression. To test this hypothesis, we developed a model of in vitro steatosis using primary hepatocytes from wild-type (WT) and UCP2 knockout (KO) mice and subjected them to hypoxia/reoxygenation (H/R). Using cultured hepatocytes treated with emulsified fatty acids for 24 h, generating a steatotic phenotype (i.e., microvesicular and broad-spectrum fatty acid accumulation), we found that the phenotype of the WT and UCP2 KO were the same; however, cellular viability was increased in the steatotic KO hepatocytes following 4 h of hypoxia and 24 h of reoxygenation; Hepatocellular ATP levels decreased during hypoxia and recovered after reoxygenation in the control and UCP2 KO steatotic hepatocytes but not in the WT steatotic hepatocytes; mitochondrial membrane potential in WT and UCP2 KO steatotic groups was less than control groups but higher than UCP2 KO hepatocytes. Following reoxygenation, lipid peroxidation, as measured by thiobarbituric acid reactive substances, increased in all groups but to a greater extent in the steatotic hepatocytes, regardless of UCP2 expression. These results demonstrate that UCP2 sensitizes steatotic hepatocytes to H/R through mitochondrial depolarization and ATP depletion but not lipid peroxidation.

scholarly journals Down-Regulation of Replication Factor C-40 (RFC40) Causes Chromosomal Missegregation in Neonatal and Hypertrophic Adult Rat Cardiac Myocytes

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39009 ◽  
Author(s):  
Hirotaka Ata ◽  
Deepa Shrestha ◽  
Masahiko Oka ◽  
Rikuo Ochi ◽  
Chian Ju Jong ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Replication Factor C ◽  
Down Regulation ◽  
Replication Factor ◽  
Adult Rat ◽  
Factor C ◽  
Rat Cardiac Myocytes

Effects of fatty acids on uncoupling protein‐2 expression in the rat heart

2000 ◽  
Vol 14 (3) ◽  
pp. 495-502 ◽  
Author(s):  
KARIN A. J. M. VAN DER LEE ◽  
PETER H. M. WILLEMSEN ◽  
GER J. VAN DER VUSSE ◽  
MARC VAN BILSEN
Keyword(s):  
Fatty Acids ◽  
Rat Heart ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2

Effect of Napip on K0 activation of the Na-K pump in adult rat cardiac myocytes

1994 ◽  
Vol 266 (1) ◽  
pp. C37-C41 ◽  
Author(s):  
T. A. Kinard ◽  
X. Y. Liu ◽  
S. Liu ◽  
J. R. Stimers
Keyword(s):  
Environmental Factors ◽  
Cardiac Myocytes ◽  
Pump Current ◽  
Apparent Affinity ◽  
Adult Rat ◽  
Cyclic Model ◽  
Pump Activity ◽  
Dose Dependent ◽  
Rat Cardiac Myocytes ◽  
External K

To determine if environmental factors influence the external K (K0) dependence of Na-K pump current (Ip), we systematically varied internal (pipette) Na (Napip) and Na-K pump activity while measuring the K0 dependence in adult rat cardiac myocytes. For each Napip, reactivation of Ip by K0 was dose dependent. The maximal Ip (Ipmax) and apparent affinity for K0 binding to the Na-K pump (K0.5) increased as Napip increased. The results of making an equimolar substitution of tetramethylammonium for K and Cs, and partial Ip inhibition with ouabain, also showed that Ipmax and K0.5 increased as Napip increased. We simulated pump activity as a function of intracellular Na (Nai) and K0 using a cyclic model of the Na-K pump and found that the model predicts K0.5 for K0 binding increases as Na increases, even when the conditions are adjusted by removing pipette K and partial pump inhibition with ouabain.

Effects of Saponin Monomer 13 of Dwarf Lilyturf Tuber on L-Type Calcium Currents in Adult Rat Ventricular Myocytes

2005 ◽  
Vol 33 (05) ◽  
pp. 797-806 ◽  
Author(s):  
Jin Tao ◽  
Hongyi Wang ◽  
Jiandong Chen ◽  
Huae Xu ◽  
Shengnan Li
Keyword(s):  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Calcium Currents ◽  
Inhibitory Effects ◽  
Patch Clamp Recording ◽  
Inactivation Curve ◽  
Control Value ◽  
Adult Rat ◽  
Cardioprotective Effects ◽  
Rat Cardiac Myocytes

The saponin monomer 13 of dwarf lilyturf tuber (DT-13), one of the saponin monomers of dwarf lilyturf tuber, has been found to have potent cardioprotective effects. In order to investigate the effect of DT-13 on L-type calcium currents ( I Ca,L ), exploring the mechanisms of DT-13's cardioprotective effects, we directly measured the I Ca,L in the adult rat cardiac myocytes exposed to DT-13 using standard whole-cell patch-clamp recording technique. Our results showed that DT-13 exerted inhibitory effects on the I Ca,L of the single adult rat cardiac myocytes. The current density was reduced by about 38% after exposure of the cells to DT-13 (0.1 μM) for 10 minutes, from the control value of 7.46 ± 1.31 pA/pF to 4.25 ± 0.35 pA/pF ( n = 6, p < 0.05). This I Ca,L -inhibiting action of DT-13 was concentration-dependent. DT-13 up-shifted the current-voltage (I-V) curve, but did not significantly affect the half activation potential (V0.5). V0.5 was from -11.8 ± 0.9 mV in the control to -12.6 ± 1.9 mV in the presence of DT-13 at 0.1 μmol/L. DT-13 at 0.1 μM did not markedly affect the activation of I Ca,L , but shifted the inactivation curve of I Ca,L to the left. In combination with previous reports, these results suggest that there might be a close relationship between the cardioprotective effects of dwarf lilyturf tuber and the inhibitory effects of DT-13 on L-type calcium currents.

Oxidation of myoglobin in isolated adult rat cardiac myocytes by 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid

FEBS Letters ◽  
1983 ◽  
Vol 163 (2) ◽  
pp. 292-296 ◽  
Author(s):  
Frederick P. Walters ◽  
Frances G. Kennedy ◽  
Dean P. Jones
Keyword(s):  
Cardiac Myocytes ◽  
Eicosatetraenoic Acid ◽  
Adult Rat ◽  
Rat Cardiac Myocytes
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