Abstract
BackgroundStroke can induce cardiac dysfunction in the absence of primary cardiac disease; however, the mechanisms underlying the interaction between the neurological deficits and the heart are poorly understood. The objective of this study was to investigate the effects of stroke on cardiac function and to identify the transcriptome characteristics of the heart.ResultsStroke significantly decreased heart weight/tibia length ratio and cardiomyocyte cross-sectional areas and increased atrogin-1 and the E3 ubiquitin ligase MuRF-1, indicating myocardial atrophy in MCAO-induced mouse hearts. RNA sequencing of mRNA revealed 383 differentially expressed genes (DEGs) in MCAO myocardium, of which 221 were downregulated and 162 upregulated. Grouping of DEGs based on biological function and quantitative PCR validation indicated that suppressed immune response and collagen synthesis and altered activity of oxidoreductase, peptidase, and endopeptidase may be involved in MCAO-induced cardiomyopathy. The DEGs were mainly distributed in the membrane or extracellular region of cardiomyocytes and acted as potential mediators of stroke-induced cardiac dysregulation involved in cardiac atrophy.ConclusionStroke induced a unique transcriptome response in the myocardium and resulted in immediate cardiac atrophy and dysfunction.
Highlights
Cardiovascular and cerebrovascular diseases remain among the primary causes of death and medical costs worldwide [1], and share several risk factors [2]
New and noteworthy Our study revealed three new major findings: (1) experimental induced stroke caused cardiac dysfunction, (2) atrophic phenotype of the heart occurred after induced stroke, and (3) a unique myocardial mRNA expression profile was produced after induced stroke in mice
It is well known that cardiogenic strokes contribute to the occurrence of ischemic stroke [3], increasing evidence suggest that elevated cardiac troponin [4] and left atrial enlargement [5] occur in patients with stroke
Summary
Cardiovascular and cerebrovascular diseases remain among the primary causes of death and medical costs worldwide [1], and share several risk factors [2]. It is well known that cardiogenic strokes contribute to the occurrence of ischemic stroke [3], increasing evidence suggest that elevated cardiac troponin [4] and left atrial enlargement [5] occur in patients with stroke. These cardiac biomarkers (cardiac troponin and left atrial diameter) are associated with the presence of large vessel occlusions [6]. Stroke can induce cardiac dysfunction in the absence of primary cardiac disease; the mechanisms underlying the interaction between the neurological deficits and the heart are poorly understood. The objective of this study was to investigate the effects of stroke on cardiac function and to identify the transcriptome characteristics of the heart
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