YUAN SONG^1,#, CAI WEI^2,#, JINGJING WANG^3,*

BIOCELL, Vol.45, No.3, pp. 733-744, 2021, DOI:10.32604/biocell.2021.013236 - 03 March 2021

Abstract Oxidative stress-mediated cell death in cardiomyocytes contributes to the development of atrial fibrillation. However, the detailed mechanisms are still unclear. In the present study, we established atrial fibrillation models in mice. The cardiomyocytes were isolated from atrial fibrillation mice and normal mice and were cultured in vitro, respectively. The results showed that cell proliferation and viability in cardiomyocytes with atrial fibrillation were significantly lower than the cells from the normal mice. Consistently, atrial fibrillation cardiomyocytes were prone to suffer from apoptotic cell death. Also, the oxidative stress and ferroptosis-associated signatures were significantly increased in atrial… More >

ZHAOHUI HU^1,2, XIANGJUN DING³, YUYAO JI², XIAOHONG LIU^4,*, ZHIWEN DING^2,*

BIOCELL, Vol.45, No.3, pp. 745-749, 2021, DOI:10.32604/biocell.2021.013293 - 03 March 2021

Abstract Apurine/pyrimidine-free endonuclease 1 (APEX1) is a multifunctional enzyme that contributes to oxidizationmediated DNA-cleaved base excision repair and redox activation of transcription factors. However, the role of APEX1 during cardiomyocyte oxidative stress injury is not completely understood. In the present study, whether APEX1 protects oxidative damage-induced cardiomyocytes was investigated. mRNA and protein expression levels of APEX1 were downregulated in the mouse model of cardiac ischemia-reperfusion injury. Furthermore, the expression of APEX1 in hydrogen peroxide (H₂O₂)-treated neonatal mice cardiomyocytes was also decreased. APEX1 knockdown aggravated H₂O₂-treated cardiomyocyte apoptosis indexes. By contrast, APEX1 overexpression reversed H₂O₂-induced oxidative damage, as demonstrated More >

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

BIOCELL, Vol.44, No.3, pp. 371-379, 2020, DOI:10.32604/biocell.2020.08893 - 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 More >

Philip M. Tan¹, Kyle S. Buchholz², Shulin Cao², Yasser Aboelkassem², Jeffrey H. Omens², Andrew D. McCulloch^2,*, Jeffrey J. Saucerman¹

Molecular & Cellular Biomechanics, Vol.16, Suppl.1, pp. 1-3, 2019, DOI:10.32604/mcb.2019.05693

Abstract In this article, we summarize our systems model of cardiomyocyte mechano-signaling published in PLoS Computational Biology and discuss new approaches to extending these models to predict cardiac myocyte gene expression in response to stretch. More >

Sandra Deitch^∗, Bruce Z. Gao^†, Delphine Dean^‡

Molecular & Cellular Biomechanics, Vol.9, No.3, pp. 227-250, 2012, DOI:10.3970/mcb.2012.009.227

Abstract Cardiomyocyte phenotype changes significantly in 2D culture systems depending on the substrate composition and organization. Given the variety of substrates that are used both for basic cardiac cell culture studies and for regenerative medicine applications, there is a critical need to understand how the different matrices influence cardiac cell mechanics. In the current study, the mechanical properties of neonatal rat cardiomyocytes cultured in a subconfluent layer upon aligned and unaligned collagen and fibronectin matrices were assessed over a two week period using atomic force microscopy. The elastic modulus was estimated by fitting the Hertz model… More >