Unexpected Cardiac Hypertrophy by Epidermal Growth Factor Receptor Silencing

Eguchi, Akito; Eguchi, Satoru; Tilley, Douglas G.

doi:10.1161/hypertensionaha.113.01184

Cited by 2 publications

(2 citation statements)

References 5 publications

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“…EGF–receptor transactivation and dysregulation is involved in myocardial hypertrophy and contraction ( Eguchi et al, 2013 ; Xu et al, 2014 ). In an animal model, EGF–receptor phosphorylation led to tyrosine phosphorylation of cardiac Na(+) and L-type Ca(2+) channels and thus modulated electrical excitability of the heart and ischemia/reperfusion associated cardiac arrhythmia ( Feng et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of Central Regulators of Calcium Signaling and ECM–Receptor Interaction Genetically Associated With the Progression and Recurrence of Atrial Fibrillation

et al. 2018

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Atrial fibrillation (AF) is a multifactorial disease with a strong genetic background. It is assumed that common and rare genetic variants contribute to the progression and recurrence of AF. The pathophysiological impact of those variants, especially when they are synonymous or non-coding, is often elusive and translation into functional experiments is difficult. In this study, we propose a method to go straight from genetic variants to defined gene targets. We focused on 55 genes from calcium signaling and 26 genes from extra cellular matrix ECM–receptor interaction that we found to be associated with the progression and recurrence of AF. These genes were mapped on protein–protein interaction data from three different databases. Based on the concept that central regulators are highly connected with their neighbors, we identified central hub proteins according to random walk analysis derived scores representing interaction grade. Our approach resulted in the identification of EGFR, RYR2, and PRKCA (calcium signaling) and FN1 and LAMA1 (ECM–receptor interaction) which represent promising targets for further functional characterization or pharmaceutical intervention.

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Section: Discussionmentioning

confidence: 99%

Identification of Central Regulators of Calcium Signaling and ECM–Receptor Interaction Genetically Associated With the Progression and Recurrence of Atrial Fibrillation

et al. 2018

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“…In this study, the reciprocal expression of several catabolic genes was also validated by qPCR ( Table 1 ). Genes involved in FoxO signaling and focal adhesion pathways, such as FoxO1 [ 76 ], caveolin 1 [ 77 ], FYN proto-oncogene [ 78 ], and epidermal growth factor receptor [ 79 ], negatively regulate muscle hypertrophy.…”

Section: Resultsmentioning

confidence: 99%

Coding and Noncoding Genes Involved in Atrophy and Compensatory Muscle Growth in Nile Tilapia

Ali

Shaalan

Al-Tobasei

et al. 2022

Cells

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Improvements in growth-related traits reduce fish time and production costs to reach market size. Feed deprivation and refeeding cycles have been introduced to maximize aquaculture profits through compensatory growth. However, the molecular compensatory growth signature is still uncertain in Nile tilapia. In this study, fish were subjected to two weeks of fasting followed by two weeks of refeeding. The growth curve in refed tilapia was suggestive of a partial compensatory response. Transcriptome profiling of starved and refed fish was conducted to identify genes regulating muscle atrophy and compensatory growth. Pairwise comparisons revealed 5009 and 478 differentially expressed (differential) transcripts during muscle atrophy and recovery, respectively. Muscle atrophy appears to be mediated by the ubiquitin-proteasome and autophagy/lysosome systems. Autophagy-related 2A, F-box and WD repeat domain containing 7, F-box only protein 32, miR-137, and miR-153 showed exceptional high expression suggesting them as master regulators of muscle atrophy. On the other hand, the muscle compensatory growth response appears to be mediated by the continuous stimulation of muscle hypertrophy which exceeded normal levels found in control fish. For instance, genes promoting ribosome biogenesis or enhancing the efficiency of translational machinery were upregulated in compensatory muscle growth. Additionally, myogenic microRNAs (e.g., miR-1 and miR-206), and hypertrophy-associated microRNAs (e.g., miR-27a-3p, miR-29c, and miR-29c) were reciprocally expressed to favor hypertrophy during muscle recovery. Overall, the present study provided insights into the molecular mechanisms regulating muscle mass in fish. The study pinpoints extensive growth-related gene networks that could be used to inform breeding programs and also serve as valuable genomic resources for future mechanistic studies.

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Unexpected Cardiac Hypertrophy by Epidermal Growth Factor Receptor Silencing

Cited by 2 publications

References 5 publications

Identification of Central Regulators of Calcium Signaling and ECM–Receptor Interaction Genetically Associated With the Progression and Recurrence of Atrial Fibrillation

Identification of Central Regulators of Calcium Signaling and ECM–Receptor Interaction Genetically Associated With the Progression and Recurrence of Atrial Fibrillation

Coding and Noncoding Genes Involved in Atrophy and Compensatory Muscle Growth in Nile Tilapia

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