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P6353Iron depletion in human cardiomyocytes cultured with sera from myocarditis patients
Abstract Background Cardiac myocytes, which are particularly sensitive to disordered iron homeostasis, are the main cells affected in the course of myocarditis. Iron is essential for the proper maintenance of energy metabolism but also plays key role in inflammation and ROS production. We hypothesiz...
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Published in: | European heart journal 2019-10, Vol.40 (Supplement_1) |
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Main Authors: | , , , , , , , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract
Background
Cardiac myocytes, which are particularly sensitive to disordered iron homeostasis, are the main cells affected in the course of myocarditis. Iron is essential for the proper maintenance of energy metabolism but also plays key role in inflammation and ROS production. We hypothesize that iron homeostasis might be involved in the pathophysiology of myocarditis.
Purpose
The aim of the study was to assess differences in the expression of key genes and proteins involved in iron homeostasis, cardiac malfunctioning, and protection against ROS in human cardiomyocytes (HCMs) cultured in the indirect model of myocarditis.
Methods
HCMs were cultured for 48 hours with 10% of sera from patients with acute myocarditis (n=11) and after 6 weeks of recovery, and also with sera from healthy controls (n=7). We analyzed expression of light and heavy ferritin chains [FTL, FTH], transferrin receptor 1 [TfR1], galectin 3 [LGALs3], TGFβ signaling [TGFβ1, TGFβ2, TGFβ3], glutathione peroxidase [GPX] and superoxide dismutase [SOD1] at the mRNA level using RTqPCR and at the protein level using Western bloting. We compared obtained data with the clinical characteristics of patients.
Results
In HCMs exposed to sera from myocarditis patients, in comparison to those treated with sera from healthy controls, we found a significant increase in an expression of TfR1 both at mRNA and protein level (p |
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ISSN: | 0195-668X 1522-9645 |
DOI: | 10.1093/eurheartj/ehz746.0949 |