Isoprenaline modified the lipidomic profile and reduced β-oxidation in HL-1 cardiomyocytes: In vitro model of takotsubo syndrome

Isoprenaline Lipid droplet Lipotoxicity Lipid Oxidation
DOI: 10.3389/fcvm.2022.917989 Publication Date: 2022-08-22T06:48:38Z
ABSTRACT
Recent studies have suggested a pathogenetic link between impaired mitochondria and Takotsubo syndrome (TTS), which is closely connected with catecholamine overstimulation, poor outcomes, changes in lipid metabolism. We investigated the metabolism at level of fatty acid β-oxidation intracellular lipidomic spectrum. The immortalized cell line HL-1 cardiomyocytes was used this study as an established vitro model TTS. cells were exposed to non-selective β-agonist isoprenaline (ISO) for acute (2 h) prolonged (24 periods. impact on mitochondrial adenosine 5'-triphosphate (ATP) production using real-time metabolic analysis, total content, spectrum high-performance liquid chromatography (HPLC) mass spectrometry. Furthermore, modifications selected transporters determined - polymerase chain reaction (RT-PCR) and/or Western blot techniques. By choosing wide range targets, we provide detailed overview molecular during overstimulation. present demonstrates that exposure ISO decreased ATP by up 42.2%, 86.4%. Prolonged also increased accumulation 4%. Lipid analysis showed reduced concentration cardioprotective lipotoxic molecules long-term exposure. Decreased utilization can lead higher formation molecules. Changes induce pathophysiological signaling pathways leading cardiomyocyte remodeling or apoptosis. Thus, induced excessive doses catecholamines may cause TTS contribute progression heart failure, risk after episode.
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