Cardiac hypertrophy limits infarct expansion after myocardial infarction in mice

Iismaa, Siiri E.; Li, Ming; Kesteven, Scott; Wu, Jianxin; Chan, Andrea Y.; Holman, Sara; Calvert, John W.; Haq, Ahtesham ul; Nicks, Amy M.; Naqvi, Nawazish; Husain, Ahsan; Feneley, Michael P.; Graham, Robert M.

doi:10.1038/s41598-018-24525-6

Cited by 18 publications

(17 citation statements)

References 33 publications

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“…Cardiac fibroblasts (PDGFR α + ) and endothelial cells (CD31 + ) were isolated from wild-type C57Bl/6J mouse hearts and sorted using APC-conjugated anti-PDGFR α + (eBioscience 17-1401-81) and PE-CY7-conjugated anti-CD31 (eBioscience 25-0311-82) antibodies as described previously [ 37 ]. Cardiomyocytes were isolated from wild-type C57Bl/6J mice as described previously [ 53 ].…”

Section: Methodsmentioning

confidence: 99%

Sierra: discovery of differential transcript usage from polyA-captured single-cell RNA-seq data

et al. 2020

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High-throughput single-cell RNA-seq (scRNA-seq) is a powerful tool for studying gene expression in single cells. Most current scRNA-seq bioinformatics tools focus on analysing overall expression levels, largely ignoring alternative mRNA isoform expression. We present a computational pipeline, Sierra, that readily detects differential transcript usage from data generated by commonly used polyA-captured scRNA-seq technology. We validate Sierra by comparing cardiac scRNA-seq cell types to bulk RNA-seq of matched populations, finding significant overlap in differential transcripts. Sierra detects differential transcript usage across human peripheral blood mononuclear cells and the Tabula Muris, and 3 UTR shortening in cardiac fibroblasts. Sierra is available at https://github.com/VCCRI/Sierra.

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Section: Methodsmentioning

confidence: 99%

Sierra: discovery of differential transcript usage from polyA-captured single-cell RNA-seq data

et al. 2020

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“…Echocardiography was undertaken by an operator blinded to genotype and treatment group. Procedures were performed under anesthesia, as described by Iismaa et al (2018) [24], either at baseline (one week after vehicle/tamoxifen treatment) or after four weeks of swim training and within 5 h of a swim-training session. Depth of anesthesia was adjusted in the same manner as for micromanometry.…”

Section: Echocardiographymentioning

confidence: 99%

Adaptation to exercise-induced stress is not dependent on cardiomyocyte α1A-adrenergic receptors

Kaidonis

Niu

Chan

et al. 2021

Journal of Molecular and Cellular Cardiology

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The 'fight or flight' response to physiological stress involves sympathetic nervous system activation, catecholamine release and adrenergic receptor stimulation. In the heart, this induces positive inotropy, previously attributed to the β 1 -adrenergic receptor subtype. However, the role of the α 1A -adrenergic receptor, which has been suggested to be protective in cardiac pathology, has not been investigated in the setting of physiological stress. To explore this, we developed a tamoxifen-inducible, cardiomyocyte-specific α 1A -adrenergic receptor knock-down mouse model, challenged mice to four weeks of endurance swim training and assessed cardiac outcomes. With 4-OH tamoxifen treatment, expression of the α 1A -adrenergic receptor was knocked down by 80-89%, without any compensatory changes in the expression of other adrenergic receptors, or changes to baseline cardiac structure and function. Swim training caused eccentric hypertrophy, regardless of genotype, demonstrated by an increase in heart weight/tibia length ratio (30% and 22% in vehicle-and tamoxifen-treated animals, respectively) and an increase in left ventricular end diastolic volume (30% and 24% in vehicle-and tamoxifen-treated animals, respectively) without any change in the wall thickness/chamber radius ratio. Consistent with physiological hypertrophy, there was no increase in fetal gene program (Myh7, Nppa, Nppb or Acta1) expression. In response to exercise-induced volume overload, stroke volume (39% and 30% in vehicleand tamoxifen-treated animals, respectively), cardiac output/tibia length ratio (41% in vehicle-treated animals) and stroke work (61% and 33% in vehicle-and tamoxifen-treated animals, respectively) increased, regardless of genotype. These findings demonstrate that cardiomyocyte α 1A -adrenergic receptors are not necessary for cardiac adaptation to endurance exercise stress and their acute ablation is not deleterious.

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“…Hypertrophy/polyploidization of cardiomyocytes in the unaffected regions of the left ventricle reduces short-term mortality by sustaining cardiac output [103]. In contrast to other organisms, adult mammalian hearts lack a major proliferative response involving cardiomyocyte progenitors and their contribution to sustained cardiac function is still debated.…”

Section: Acute Heart Injurymentioning

confidence: 99%

Surviving Acute Organ Failure: Cell Polyploidization and Progenitor Proliferation

Lazzeri¹,

Angelotti²,

Conte³

et al. 2019

Trends in Molecular Medicine

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Cardiac hypertrophy limits infarct expansion after myocardial infarction in mice

Cited by 18 publications

References 33 publications

Sierra: discovery of differential transcript usage from polyA-captured single-cell RNA-seq data

Sierra: discovery of differential transcript usage from polyA-captured single-cell RNA-seq data

Adaptation to exercise-induced stress is not dependent on cardiomyocyte α1A-adrenergic receptors

Surviving Acute Organ Failure: Cell Polyploidization and Progenitor Proliferation

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