Ubiquinol-cytochrome c reductase core protein 1 contributes to cardiac tolerance to acute exhaustive exercise

2021 ◽  
pp. 153537022110465
Author(s):  
Tingting Yi ◽  
Huifang Chen ◽  
Jian Zhan ◽  
Yu Li ◽  
Zonghong Long ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Structural Changes ◽  
Core Protein ◽  
Left Ventricular ◽  
Complex Iii ◽  
Exhaustive Exercise ◽  
In Vivo Models ◽  
Cytochrome C Reductase ◽  
Lv Volume

Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) is an indispensable component of mitochondrial complex III. It plays a key role in cardioprotection and maintaining mitochondrion function. However, the exact role of UQCRC1 in maintaining cardiac function has not been reported by in vivo models. Also, the exact biological functions of UQCRC1 are far from fully understood. UQCRC1+/− mice had decreased both mRNA and protein expression of UQCRC1 in the left ventricular myocardia, and these mice had reduced tolerance to acute exhaustive exercise including decreased time and distance with higher apoptosis rate, higher expression level of cleaved CASPASE 3, and higher ratio of cleaved PARP1 to full-length PARP1. Moreover, UQCRC1 knockdown led to increased LV interventricular septal thicknesses both at systole and diastole, as well as decreased LV volume both at end-systole and end-diastole. Finally, UQCRC1 gene disruption resulted in mitochondrial vacuolation, fibril disarrangement, and more severe morphological and structural changes in mitochondria after acute exhaustive exercise. In conclusion, UQCRC1 contributes to cardiac tolerance to acute exhaustive exercise in mice, and it may be an essential component of complex III, playing a crucial role in maintaining cardiac functions.

Effects of Rest and Exercise on Cardiac Blood Volume Determinations

1997 ◽  
Vol 36 (08) ◽  
pp. 259-264
Author(s):  
N. Topuzović
Keyword(s):  
Radionuclide Ventriculography ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Volume Determination ◽  
Group I ◽  
Lv Volumes ◽  
Group Ii ◽  
Lv Volume

Summary Aim: The purpose of this study was to investigate the changes in blood activity during rest, exercise and recovery, and to assess its influence on left ventricular (LV) volume determination using the count-based method requiring blood sampling. Methods: Forty-four patients underwent rest-stress radionuclide ventriculography; Tc-99m-human serum albumin was used in 13 patients (Group I), red blood cells was labeled using Tc-99m in 17 patients (Group II) in vivo, and in 14 patients (Group III) by modified in vivo/in vitro method. LV volumes were determined by a count-based method using corrected count rate in blood samples obtained during rest, peak exercise and after recovery. Results: In group I at stress, the blood activity decreased by 12.6 ± 5.4%, p <0.05, as compared to the rest level, and increased by 25.1 ± 6.4%, p <0.001, and 12.8 ± 4.5%, p <0.05, above the resting level in group II and III, respectively. This had profound effects on LV volume determinations if only one rest blood aliquot was used: during exercise, the LV volumes significantly decreased by 22.1 ± 9.6%, p <0.05, in group I, whereas in groups II and III it was significantly overestimated by 32.1 ± 10.3%, p <0.001, and 10.7 ± 6.4%, p <0.05, respectively. The changes in blood activity between stress and recovery were not significantly different for any of the groups. Conclusion: The use of only a single blood sample as volume aliquot at rest in rest-stress studies leads to erroneous estimation of cardiac volumes due to significant changes in blood radioactivity during exercise and recovery.

scholarly journals Membrane topology of beef-heart ubiquinone-cytochrome c reductase (complex III).

1981 ◽  
Vol 256 (21) ◽  
pp. 11132-11136 ◽  
Author(s):  
H. Gutweniger ◽  
R. Bisson ◽  
C. Montecucco
Keyword(s):  
Cytochrome C ◽  
Membrane Topology ◽  
Complex Iii ◽  
Beef Heart ◽  
Cytochrome C Reductase

scholarly journals Overexpression of Ubiquinol-Cytochrome c Reductase Core Protein 1 May Protect H9c2 Cardiac Cells by Binding with Zinc

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Tingting Yi ◽  
Xiaoxiao Wu ◽  
Zonghong Long ◽  
Guangyou Duan ◽  
Zhuoxi Wu ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Caspase 3 ◽  
Direct Evidence ◽  
Core Protein ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Protective Effects ◽  
Cytochrome C Reductase ◽  
Simulated Ischemia

In several recent studies, proteomics analyses suggest that increase of ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) is cardio-protective. However, direct evidence for this effect has not yet been obtained. Thus, the current study aimed to determine this effect and the mechanism underlying this effect. The results showed that overexpression of UQCRC1 protected H9c2 cardiac cells against in vitro simulated ischemia-reperfusion by maintaining mitochondrial membrane potential and suppressing the expression of caspase-3. These protective effects were significantly enhanced by exogenous Zn2+ but completely abolished by Zn2+-selective chelator TPEN. Furthermore, the upregulation of UQCRC1 reduced the concentration of free Zn2+ in mitochondria, whereas the downregulation of UQCRC1 increased the concentration of free Zn2+ in mitochondria. In conclusion, the overexpression of UQCRC1 can protect H9c2 cardiac cells against simulated ischemia/reperfusion, and this cardio-protective effect is likely mediated by zinc binding.

scholarly journals Cytochrome c-mediated electron transfer between ubiquinol-cytochrome c reductase and cytochrome c oxidase. Kinetic evidence for a mobile cytochrome c pool

1984 ◽  
Vol 217 (2) ◽  
pp. 551-560 ◽  
Author(s):  
R J Froud ◽  
C I Ragan
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
State Level ◽  
Complex Iii ◽  
Molar Ratio ◽  
Cytochrome C Reductase ◽  
Molar Ratios ◽  
Ubiquinol Oxidase ◽  
Mediated Electron Transfer ◽  
Pool Model

Ubiquinol oxidase has been reconstituted from ubiquinol-cytochrome c reductase (Complex III), cytochrome c and cytochrome c oxidase (Complex IV). The steady-state level of reduction of cytochrome c by ubiquinol-2 varies with the molar ratios of the complexes and with the presence of antimycin in a way that can be quantitatively accounted for by a model in which cytochrome c acts as a freely diffusible pool on the membrane. This model was based on that of Kröger & Klingenberg [(1973) Eur. J. Biochem. 34, 358-368] for ubiquinone-pool behaviour. Further confirmation of the pool model was provided by analysis of ubiquinol oxidase activity as a function of the molar ratio of the complexes and prediction of the degree of inhibition by antimycin.

Ubiquinol–cytochrome-c reductase 7.2 kDa protein of mitochondrial complex III is steroid-responsive and increases in cardiac hypertrophy and hypertension

2007 ◽  
Vol 85 (10) ◽  
pp. 986-996 ◽  
Author(s):  
Hung Huynh ◽  
Nicolas Servant ◽  
Lorraine E. Chalifour
Keyword(s):  
Cytochrome C ◽  
Cardiac Hypertrophy ◽  
Premenopausal Women ◽  
Complex Iii ◽  
Ovariectomized Rats ◽  
Spontaneously Hypertensive ◽  
Cytochrome C Reductase ◽  
Mitochondrial Respiratory Complex ◽  
Wistar Kyoto ◽  
Intact Rats

Women and men do not respond identically to cardiac insults; premenopausal women are somewhat protected from cardiovascular disease. Our objective was to isolate and characterize hormone-responsive genes in the heart. Differential display identified an estrogen-inducible fragment that was found to encode the ubiquinol–cytochrome-c reductase (UCCR) 7.2 kDa protein of the mitochondrial respiratory complex III. We found UCCR7.2 mRNA to be highly expressed in the heart, and this expression increased in hearts of 4-, 10-, and 28-week-old spontaneously hypertensive rats (SHR) compared with normotensive Wistar–Kyoto rats. Oral hydralazine treatment to reduce hypertension reduced SHR UCCR7.2 expression. Cardiac UCCR7.2 mRNA expression was also increased significantly after a 5/6 nephrectomy compared with mock surgery. Cardiac expression after ovariectomy was 50% that of intact rats. Supplementation of ovariectomized rats with estrogen had no effect, whereas progesterone increased cardiac expression, although not to intact levels. No change in cardiac UCCR7.2 expression was found when intact rats were treated with either tamoxifen or ICI 182780. Thus, UCCR7.2 expression is reduced in the absence of ovarian hormones, but is not directly regulated by estrogen in the heart. We conclude that UCCR7.2 is a steroid hormone-responsive gene in the heart, with expression increased in cardiac hypertrophy and in response to hypertension.

A mitochondrial cytochrome b mutation but no mutations of nuclearly encoded subunits in ubiquinol cytochrome c reductase (complex III) deficiency

1999 ◽  
Vol 104 (6) ◽  
pp. 460-466 ◽  
Author(s):  
Isabelle Valnot ◽  
Johanna Kassis ◽  
Dominique Chretien ◽  
Pascale de Lonlay ◽  
Béatrice Parfait ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cytochrome B ◽  
Complex Iii ◽  
Mitochondrial Cytochrome ◽  
Cytochrome C Reductase ◽  
Mitochondrial Cytochrome B

scholarly journals Cardiac Electrical and Structural Changes During Bacterial Infection: An Instructive Model to Study Cardiac Dysfunction in Sepsis

2016 ◽  
Vol 5 (9) ◽  
Author(s):  
Michael A. Makara ◽  
Ky V. Hoang ◽  
Latha P. Ganesan ◽  
Elliot D. Crouser ◽  
Mahmood Khan ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Structural Changes ◽  
Immune Cell ◽  
Left Ventricular ◽  
Infection Model ◽  
Myocardial Inflammation ◽  
Multiple Time ◽  
Heat Shock Factor 1 ◽  
Cardiac Damage

Background Sepsis patients with cardiac dysfunction have significantly higher mortality. Although several pathways are associated with myocardial damage in sepsis, the precise cause(s) remains unclear and treatment options are limited. This study was designed to develop a new model to investigate the early events of cardiac damage during sepsis progression. Methods and Results Francisella tularensis subspecies novicida ( Ft.n ) is a Gram‐negative intracellular pathogen causing severe sepsis syndrome in mice. BALB /c mice (N=12) were sham treated or infected with Ft.n through the intranasal route. Serial electrocardiograms were recorded at multiple time points until 96 hours. Hearts were then harvested for histology and gene expression studies. Similar to septic patients, we illustrate both cardiac electrical and structural phenotypes in our murine Ft.n infection model, including prominent R' wave formation, prolonged QRS intervals, and significant left ventricular dysfunction. Notably, in infected animals, we detected numerous microlesions in the myocardium, previously observed following nosocomial Streptococcu s infection and in sepsis patients. We show that Ft.n ‐mediated microlesions are attributed to cardiomyocyte apoptosis, increased immune cell infiltration, and expression of inflammatory mediators (tumor necrosis factor, interleukin [ IL] ‐1β, IL ‐8, and superoxide dismutase 2). Finally, we identify increased expression of microRNA‐155 and rapid degradation of heat shock factor 1 following cardiac Ft.n infection as a primary cause of myocardial inflammation and apoptosis. Conclusions We have developed and characterized an Ft.n infection model to understand the pathogenesis of cardiac dysregulation in sepsis. Our findings illustrate novel in vivo phenotypes underlying cardiac dysfunction during Ft.n infection with significant translational impact on our understanding of sepsis pathophysiology.

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