Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction

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Title: Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction
Authors: Veltkamp, R
Uhlmann, S
Marinescu, M
Sticht, C
Finke, D
Gretz, N
Groene, H-J
Katus, HA
Backs, J
Lehmann, LH
Item Type: Journal Article
Abstract: Background Stroke can lead to cardiac dysfunction in patients, but the mechanisms underlying the interaction between the injured brain and the heart are poorly understood. The objective of the study is to investigate the effects of experimental murine stroke on cardiac function and molecular signalling in the heart. Methods and results Mice were subjected to filament‐induced left middle cerebral artery occlusion for 30 or 60 min or sham surgery and underwent repetitive micro‐echocardiography. Left ventricular contractility was reduced early (24–72 h) but not late (2 months) after brain ischaemia. Cardiac dysfunction was accompanied by a release of high‐sensitive cardiac troponin (hsTNT (ng/ml): d1: 7.0 ± 1.0 vs. 25.0 ± 3.2*; d3: 7.3 ± 1.1 vs. 52.2 ± 16.7*; d14: 5.7 ± 0.8 vs. 5.2 ± 0.3; sham vs. 60 min. MCAO; mean ± SEM; *p < 0.05); reduced heart weight (heart weight/tibia length ratio: d1: 6.9 ± 0.2 vs. 6.4 ± 0.1*; d3: 6.7 ± 0.2 vs. 5.8 ± 0.1*; d14: 6.7 ± 0.2 vs. 6.4 ± 03; sham vs. 60 min. MCAO; mean ± SEM; *p < 0.05); resulting from cardiomyocyte atrophy (cardiomyocyte size: d1: 12.8% ± 0.002**; d3: 13.5% ± 0.002**; 14d: 6.3% ± 0.003*; 60 min. MCAO vs. sham; mean ± SEM; **p < 0.01; *p < 0.05), accompanied by increased atrogin‐1 and the E3 ubiquitin ligase murf‐1. Net norepinephrine but not synthesis was increased, suggesting a reduced norepinephrine release or an increase of norepinephrine re‐uptake, resulting in a functional denervation. Transcriptome analysis in cardiac tissue identified the transcription factor peroxisome proliferator‐activated receptor gamma as a potential mediator of stroke‐induced transcriptional dysregulation involved in cardiac atrophy. Conclusions Stroke induces a complex molecular response in the heart muscle with immediate but transient cardiac atrophy and dysfunction.
Issue Date: 1-Feb-2019
Date of Acceptance: 28-Jun-2018
URI: http://hdl.handle.net/10044/1/70541
DOI: https://doi.org/10.1002/jcsm.12335
ISSN: 2190-6009
Publisher: Wiley Open Access
Start Page: 54
End Page: 62
Journal / Book Title: Journal of Cachexia, Sarcopenia and Muscle
Volume: 10
Issue: 1
Copyright Statement: © 2018 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society on Sarcopenia, Cachexia and Wasting Disorders Journal of Cachexia, Sarcopenia and Muscle 2019; 10: 54–62 Published online 30 October 2018 in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/jcsm.12335. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes (https://creativecommons.org/licenses/by-nc/4.0/).
Sponsor/Funder: St Marys Development Trust
Funder's Grant Number: RE:SOBELL CHAIR
Keywords: Science & Technology
Life Sciences & Biomedicine
Geriatrics & Gerontology
Medicine, General & Internal
General & Internal Medicine
Ischaemic stroke
Cardiac dysfunction
Atrophy
Cardiomyocytes
Left ventricular contractility
NERVOUS-SYSTEM
FOCAL ISCHEMIA
HEART
EXPRESSION
GAMMA
CARDIOMYOPATHY
KNOCKOUT
BRAIN
Atrophy
Cardiac dysfunction
Cardiomyocytes
Ischaemic stroke
Left ventricular contractility
Science & Technology
Life Sciences & Biomedicine
Geriatrics & Gerontology
Medicine, General & Internal
General & Internal Medicine
Ischaemic stroke
Cardiac dysfunction
Atrophy
Cardiomyocytes
Left ventricular contractility
NERVOUS-SYSTEM
FOCAL ISCHEMIA
HEART
EXPRESSION
GAMMA
CARDIOMYOPATHY
KNOCKOUT
BRAIN
Publication Status: Published
Online Publication Date: 2018-10-30
Appears in Collections:Department of Medicine
Faculty of Medicine



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