Open Access

ARTICLE

YB-1 downregulation attenuates UQCRC1 protein expression level in H9C2 cells and decreases the mitochondrial membrane potential

HUIFANG CHEN^1,2, XIAOYING ZHOU², ZONGHONG LONG², XIANGLONG TANG², HONG LI^2,*

1 Department of Radiology, Chongqing University Cancer Hospital & Chongqing Cancer Institute & Chongqing Cancer Hospital, Chongqing, China
2 Department of Anesthesiology, The Second Affiliated Hospital of Army Military Medical University, Chongqing, 400037, China

* Address correspondence to: Hong Li,

BIOCELL 2020, 44(3), 371-379. https://doi.org/10.32604/biocell.2020.08893

Received 23 October 2019; Accepted 21 April 2020; Issue published 22 September 2020

Abstract

UQCRC1 is one of the 10 mitochondrial complex III subunits, this protein has a role in energy metabolism, myocardial protection, and neurological diseases. The upstream mechanism of the UQCRC1 protective effect on cardiomyocytes is currently unavailable. In order to explore the upstream molecules of UQCRC1 and elucidate the protective mechanism of UQCRC1 on cardiomyocytes in more detail, we focused on the nuclease-sensitive elementbinding protein 1 (YB-1). We hypothesized YB-1 acts as an upstream regulatory molecule of UQCRC1. This study found that YB-1 RNAi significantly reduces the expression of the UQCRC1 protein level (p < 0.05) and obviously decreases the mitochondrial membrane potential (p < 0.05), and that YB-1 interacts with UQCRC1 protein in vivo, but YB-1 RNAi has little effect on the UQCRC1 gene transcription.

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