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The aim of this study was to investigate the mechanism of cellular regulation of mitochondrial respiration in permeabilized cardiac cells with clearly different structural organization: (i) in isolated rat cardiomyocytes with very regular mitochondrial arrangement, (ii) in HL-1 cells from mouse heart, and (iii) in non-beating (NB HL-1 cells) without sarcomeres with irregular and dynamic filamentous mitochondrial network. We found striking differences in the kinetics of respiration regulation by exogenous ADP between these cells: the apparent Km for exogenous ADP was by more than order of magnitude (14 times) lower in the permeabilized non-beating NB HL-1 cells without sarcomeres (25+/-4 microM) and seven times lower in normally cultured HL-1 cells (47+/-15 microM) than in permeabilized primary cardiomyocytes (360+/-51 microM). In the latter cells, treatment with trypsin resulted in dramatic changes in intracellular structure that were associated with 3-fold decrease in apparent Km for ADP in regulation of respiration. In contrast to permeabilized cardiomyocytes, in NB HL-1 cells creatine kinase activity was low and the endogenous ADP fluxes from MgATPases recorded spectrophotometrically by the coupled enzyme assay were not reduced after activation of mitochondrial oxidative phosphorylation by the addition of mitochondrial substrates, showing the absence of ADP channelling in the NB HL-1 cells. While in the permeabilized cardiomyocytes creatine strongly activated mitochondrial respiration even in the presence of powerful competing pyruvate kinase-phosphoenolpyruvate system, in the NB HL-1 cells the stimulatory effect of creatine was not significant. The results of this study show that in normal adult cardiomyocytes and HL-1 cells intracellular local restrictions of diffusion of adenine nucleotides and metabolic feedback regulation of respiration via phosphotransfer networks are different, most probably related to differences in structural organization of these cells.
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http://dx.doi.org/10.1016/j.bbabio.2006.09.008 | DOI Listing |
Zhongguo Zhong Yao Za Zhi
October 2024
Institute of Basic Medicine, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China National Clinical Research Center for Chinese Medicine Cardiology Beijing 100091, China.
This study investigated the mechanism by which ginsenoside Rg_(1 )attenuates hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes by inhibiting the acetylation of ATP synthase subunit alpha(ATP5A1) through silent information regulator 3(SIRT3). In this study, an H/R injury model was constructed by hypoxia for 6 h and reoxygenation for 2 h in HL-1 cardiomyocytes. First, the optimal effective concentration of ginsenoside Rg_1 was determined using a cell viability assay kit.
View Article and Find Full Text PDFJ Mol Cell Cardiol
December 2024
Cardiac Pacing and Electrophysiology Department, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China; Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China. Electronic address:
Objectives: To investigate the role and mechanism of MAPK14/AIFM2 pathway in Ang II-induced atrial fibrillation in rats.
Methods: A rat model of AF was established for in vivo experiments and HL-1 cells were treated with Ang II to develop an in vitro model. In addition, HL1 cells overexpressing AIFM2 (oeAIFM2) were constructed.
Biomol Biomed
November 2024
Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Division of Cardiology, Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Discov Med
November 2024
Department of Cardiology, The 82nd Group Army Hospital of the Chinese PLA, 071000 Baoding, Hebei, China.
Background: Hypoxia has a major regulatory impact on the electrical activity transmission in the myocardium, and it is involved in the development of tachyarrhythmia disease. Anchor protein G (ankyrin-G, ANK-G) is associated with voltage-gated Na channels (Nav1.5), but its specific role and mechanism have not been fully defined.
View Article and Find Full Text PDFPharmaceuticals (Basel)
November 2024
Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.
Unlabelled: Background: Rising global temperatures have been linked to an increased incidence of heat stress (HS)-induced myocardial damage.
Methods: This study aimed to investigate the therapeutic potential of shikimic acid (SA) on HS-induced myocardial damage using network pharmacology, molecular docking, molecular dynamics (MD) simulations, and in vitro experiments.
Results: Network pharmacology analysis indicated that SA significantly attenuates the inflammatory response to HS by modulating 60 targets, including TNF, IL-6, and STAT3, which are enriched in the PI3K/AKT signaling pathway.
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