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Altered cardiac gene expression of noradrenaline enzymes, transporter and beta-adrenoceptors in rat model of rheumatoid arthritis

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2017
Authors
Dronjak, Slađana
Stefanović, Bojana
Jovanović, Predrag
Spasojević, Nataša
Jankovic, Milica
Jeremic, Ivica
Hoffmann, Markus
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Abstract
Baseline sympathetic activity was found to be elevated in rheumatoid arthritis (RA) patients and it is related to increased cardiovascular risk in these patients. Although many studies have highlighted the association between RA and increased cardiac sympathetic activity, the underlying mechanistic links remain unclear. The aim of the present study was to understand how diseases-triggered changes in gene expression may result in maladaptive physiological changes. Our results suggest that the equilibrium between noradrenaline synthesis, release and reuptake was disrupted in the ventricles of arthritic rats. In the acute phase of the arthritic process, decreased gene expression of MAO-A might lead to accumulation of noradrenaline in myocardial interstitial space, whereas increased gene expression of NET protected cardiomyocytes from the deleterious effects of enhanced noradrenaline. During the chronic phase, reduced expression of beta(1)-adrenoceptor and decreased efficiency of noradrena...line reuptake contribute to progressive damage of the myocardium and limits heart efficiency.

Keywords:
Pristane / Rheumatoid arthritis / Heart ventricles / Noradrenaline / Gene expression / Rats
Source:
Autonomic Neuroscience: Basic and Clinical, 2017, 208, 165-169
Projects:
  • Molecular mechanisms of cellular responses on pathological changes in central neuronal system and peripheral organs of mammals (RS-173044)

DOI: 10.1016/j.autneu.2017.10.003

ISSN: 1566-0702 (print); 1872-7484 (electronic)

PubMed: 29029974

WoS: 000423642600023

Scopus: 2-s2.0-85030841700
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URI
http://vinar.vin.bg.ac.rs/handle/123456789/1929
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Vinča

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