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

Yi, Tingting; Wu, Xiaoxiao; Long, Zai-Yun; Duan, Guangyou; Wu, Zhuoxi; Li, Hong; Chen, Huifang; Zhou, Xiaoying

doi:10.1155/2017/1314297

Cited by 10 publications

(7 citation statements)

References 38 publications

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“…These results indicate the association of UQCRC1 expression change with pathological processes but are insufficient to imply its biological functions. We have shown in recent studies that UQCRC1 over-expression reduces oxygen-glucose deprivationinduced injury of rat embryonic ventricular myocytes and that silencing UQCRC1 has the opposite effects [9,10]. These results indicate a protective effect of UQCRC1 on cardiomyocyte cultures.…”

Section: Introductionmentioning

confidence: 70%

Critical role of UQCRC1 in embryo survival, brain ischemic tolerance and normal cognition in mice

Shan

et al. 2019

Cell. Mol. Life Sci.

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Ubiquinol cytochrome c reductase core protein I (UQCRC1) is a component of the complex III in the respiratory chain. Its biological functions are unknown. Here, we showed that knockout of UQCRC1 led to embryonic lethality. Disrupting one UQCRC1 allele in mice (heterozygous mice) of both sexes did not affect their growth but reduced UQCRC1 mRNA and protein in the brain. These mice had decreased complex III formation, complex III activity and ATP content in the brain at baseline. They developed worsened neurological outcome after brain ischemia/hypoxia or focal brain ischemia compared with wild-type mice. The ischemic cerebral cortex of the heterozygous mice had decreased mitochondrial membrane potential and ATP content as well as increased free radicals. Also, the heterozygous mice performed poorly in the Barnes maze and novel object recognition tests. Finally, UQCRC1 was expressed abundantly in neurons and astrocytes. These results suggest a critical role of UQCRC1 in embryo survival. UQCRC1 may also be important by forming the complex III to maintain normal brain ischemic tolerance, learning and memory.

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Section: Introductionmentioning

confidence: 70%

Critical role of UQCRC1 in embryo survival, brain ischemic tolerance and normal cognition in mice

Shan

et al. 2019

Cell. Mol. Life Sci.

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“…Specific loss of UQCRC1 in cells of epithelial origin can lead to mitochondrial dysfunction. The overexpression of UQCRC1 helps to maintain the mitochondrial function of H9C2 cells and regulates apoptosis-related proteins by mediating the PI3K/Akt/GSK-3b pathway to protect H9C2 cells from simulated ischemia/reperfusion injury ( 53 ). These studies suggest that UQCRC1 plays an important role in mitochondrial function, and may have a protective effect on cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Extensive mitochondrial proteome disturbance occurs during the early stages of acute myocardial ischemia

Wang

Fan

et al. 2021

Exp Ther Med

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Mitochondrial malfunction leads to the remodeling of myocardial energy metabolism during myocardial ischemia (MI). However, the alterations to the mitochondrial proteome profile during this period has not yet been clarified. An acute MI model was established by high position ligation of the left anterior descending artery in 8-week-old C57BL/6N mice. After 15 min of ligation, the animals were euthanized, and their hearts were collected. The myocardial ultrastructure was observed using transmission electron microscopy (TEM). The cardiac mitochondrial proteome profile was analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and bioinformatics analyses. TEM showed that the outer membrane of the mitochondria was dissolved, and the inner membrane (cristae) was corrupted and broken down extensively in the MI group. The mitochondrial membrane potential was decreased. More than 1,700 mitochondrial proteins were identified by LC-MS/MS analysis, and 119 were differentially expressed. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis showed that endopeptidase activity regulation, the mitochondrial inner membrane, oxidative phosphorylation, the hypoxia-inducible factor-1 signaling pathway, the pentose phosphate pathway and the peroxisome proliferator-activated receptor signaling pathway were involved in the pathophysiological process in the early stage of acute MI. Extensive and substantial changes in the mitochondrial proteins as well as mitochondrial microstructural damage occur in the early stages of acute MI. In the present study, the series of proteins crucially involved in the pathways of mitochondrial dysfunction and metabolism were identified. Further studies are needed to clarify the roles of these proteins in myocardial metabolism remodeling during acute MI injury.

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“…[17][18][19] Accumulating evidence shows that changes of UQCRC1 expression may directly influence mitochondria structure and function, which has been proved to be necessary to maintain mitochondrial membrane potential, complex III activity, and ATP production. 6,15,16 Any pathophysiological change or disruption of these processes may cause tissues or organs very vulnerable to injury, 4,5,35 which may be a mechanism for the decreased cardiac tolerance to AEE in UQCRC1 þ/À mice. Furthermore, disruption of one Uqcrc1 allele leads to myocardial including mitochondrial, structural damage, resulting in increased LV interventricular septal thicknesses both at systole and diastole, as well as decreased LV volume both at end-systole and end-diastole, and this may directly influence blood and energy supply and may also explain the decreased cardiac tolerance to AEE.…”

Section: Discussionmentioning

confidence: 99%

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

Chen

Zhan

et al. 2021

Exp Biol Med (Maywood)

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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.

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

Cited by 10 publications

References 38 publications

Critical role of UQCRC1 in embryo survival, brain ischemic tolerance and normal cognition in mice

Critical role of UQCRC1 in embryo survival, brain ischemic tolerance and normal cognition in mice

Extensive mitochondrial proteome disturbance occurs during the early stages of acute myocardial ischemia

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

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