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Abstract

Ubiquinol Cytochrome C Reductase Core Protein I (UQCRC1) is a vital component of mitochondrial proteins, and its aberrant expression or dysfunction may play a significant role in the onset and progression of various diseases. Our previous study demonstrated notable alterations in UQCRC1 protein levels within myocardial cells in a murine model of acute myocardial ischemia. However, there is currently a paucity of literature addressing how fluctuations in UQCRC1 protein levels influence mitochondrial function in myocardial cells.

 In this investigation, we silenced the UQCRC1 gene in rat myocardial cells under hypoxic conditions using a constructed shRNA expression vector. We employed a variety of experimental methodologies, including Hoechst staining, inverted fluorescence microscopy, electron microscopy, and CCK-8 assays, to evaluate the apoptosis rate of H9C2 cells and document pathological changes in mitochondrial ultrastructure. Furthermore, we assessed cellular viability, lactate dehydrogenase levels, reactive oxygen species, ATP expression, and alterations in mitochondrial membrane potential in H9C2 cells to gain preliminary insights into the impact of the UQCRC1 gene on mitochondrial function in hypoxic rat myocardial cells from both morphological and functional perspectives.

 Our findings elucidate the underlying mechanisms associated with the occurrence and prognosis of ischemic heart disease cardiomyopathy through the UQCRC1 pathway.

Keywords: UQCRC1, Hypoxia, Cardio myocytes, Mitochondria, Ischemic heart disease