Overexpression of Ubiquinol-Cytochrome c Reductase Core Protein 1 May Protect H9c2 Cardiac Cells by Binding with Zinc.
Tingting YiXiaoxiao WuZonghong LongGuangyou DuanZhuoxi WuHong LiHuifang ChenXiaoying ZhouPublished in: BioMed research international (2017)
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.
Keyphrases
- induced apoptosis
- cell cycle arrest
- cell proliferation
- signaling pathway
- cell death
- heavy metals
- endoplasmic reticulum stress
- oxidative stress
- poor prognosis
- binding protein
- left ventricular
- transcription factor
- mass spectrometry
- heart failure
- risk assessment
- reactive oxygen species
- protein protein
- long non coding rna
- climate change
- oxide nanoparticles