Regulation of cardiac melusin gene expression by hypertrophic stimuli in the rat

Aro, Jani; Tokola, Heikki; Ronkainen, Veli‐Pekka; Koivisto, Elina; Tenhunen, Olli; Ilves, Mika; Szokodi, István; Ruskoaho, Heikki; Rysä, Jaana

doi:10.1111/apha.12044

Cited by 7 publications

(6 citation statements)

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“…In fact, overexpression of melusin in transgenic mice has been reported to protect against dilated cardiac myopathy due to pressure overload [4]. Previous work by Aro and colleagues revealed that mechanical stress was both necessary and sufficient to increase melusin mRNA steady-state concentrations in atrial HL-1 cells [2]. This supports our current finding that exercise training elevates LV melusin mRNA concentration, and opens the door for future investigations into the use of this transcript as a biomarker for cardiac adaptations to exercise training.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we hypothesized that Arg1 mRNA concentrations would be elevated in LV 12 weeks post-MI. As for melusin transcript levels, previous work by Aro et al revealed that melusin mRNA concentration increases in atrial HL-1 cells exposed to cyclic stretching [2]. This led us to hypothesize that training would increase LV melusin mRNA concentrations.…”

Section: Introductionmentioning

confidence: 86%

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Effects of pericardiectomy on training- and myocardial infarction-induced left ventricular hypertrophy, chamber dimensions and gene expression

Wolff

Rasmussen²,

Wichern³

et al. 2016

Int J Sports Med

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The primary purpose of the study was to evaluate whether a pericardiectomy (PERI) alters training- or myocardial infarction (MI)-induced left ventricular hypertrophy (LVH), chamber geometry, gene expression and/or running performance. Mice were randomized into 6 groups: naïve control (CONT)-sedentary (Sed), CONT-trained (Tr), PERI-Sed, PERI-Tr, MI-Sed and MI-Tr. MI mice also received a pericardiectomy as part of the MI surgical procedure. 10 weeks of treadmill running resulted in enhanced running performance-to-exhaustion in all 3 trained groups (CONT-Tr, PERI-Tr, MI-Tr) compared to sedentary cohorts (<0.001). Training also resulted in similar increases in normalized LVH (LV/BW) in CONT-Tr and PERI-Tr mice. 2D-echocardiographic evaluation of LV internal chamber dimensions revealed that stroke diameter (SD) was larger in PERI compared to MI (<0.01) but not CONT mice. Ventricular B-type natriuretic peptide mRNA (BNP) was elevated only in the 2 MI groups. Left ventricle β-adrenergic receptor (β-AR) and melusin transcripts both demonstrated an overall increase in trained compared to sedentary mice (both <0.05). Additionally long-term pericardiectomy did not further enhance running performance or increase LV/BW in either sedentary or trained mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 86%

Effects of pericardiectomy on training- and myocardial infarction-induced left ventricular hypertrophy, chamber dimensions and gene expression

Wolff

Rasmussen²,

Wichern³

et al. 2016

Int J Sports Med

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“…Fresh CSFM was changed 24 h after the infection and cells were cultured in all 72 h before being washed twice with ice-cold PBS and stored at −70 °C. Endothelin-1 (ET-1) treatment was performed as described before [ 35 , 36 ].…”

Section: Methodsmentioning

confidence: 99%

“…Western blots were performed as previously described [ 35 ]. Briefly, 15–60 μg of protein was loaded onto a SDS-PAGE gel and transferred to nitrocellulose filters.…”

Section: Methodsmentioning

confidence: 99%

TSC-22 up-regulates collagen 3a1 gene expression in the rat heart

Kelloniemi

Aro

Näpänkangas

et al. 2015

BMC Cardiovasc Disord

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BackgroundThe transforming growth factor (TGF)-β is one of the key mediators in cardiac remodelling occurring after myocardial infarction (MI) and in hypertensive heart disease. The TGF-β-stimulated clone 22 (TSC-22) is a leucine zipper protein expressed in many tissues and possessing various transcription-modulating activities. However, its function in the heart remains unknown.MethodsThe aim of the present study was to characterize cardiac TSC-22 expression in vivo in cardiac remodelling and in myocytes in vitro. In addition, we used TSC-22 gene transfer in order to examine the effects of TSC-22 on cardiac gene expression and function.ResultsWe found that TSC-22 is rapidly up-regulated by multiple hypertrophic stimuli, and in post-MI remodelling both TSC-22 mRNA and protein levels were up-regulated (4.1-fold, P <0.001 and 3.0-fold, P <0.05, respectively) already on day 1. We observed that both losartan and metoprolol treatments reduced left ventricular TSC-22 gene expression. Finally, TSC-22 overexpression by local intramyocardial adenovirus-mediated gene delivery showed that TSC-22 appears to have a role in regulating collagen type IIIα1 gene expression in the heart.ConclusionsThese results demonstrate that TSC-22 expression is induced in response to cardiac overload. Moreover, our data suggests that, by regulating collagen expression in the heart in vivo, TSC-22 could be a potential target for fibrosis-preventing therapies.

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“…Melusin is a muscle specific protein that binds to the cytoplasmic domain of β1 integrin, thought to act as a mechanical stretch sensor ( Brancaccio et al, 1999 ). Melusin expression increases with various hypertrophic stimuli (cyclic mechanical stretch, angiotensin-II, endothelin-1, and phenelyphrine) in neonatal ventricular cardiomyocytes in vitro ( Aro et al, 2013 ), suggesting a direct role in cardiac hypertrophy. In vivo studies performed with Melusin -null mice subjected to pressure overload demonstrated reduced left ventricular hypertrophy, accelerated development of dilated cardiomyopathy and contractile dysfunction ( Brancaccio et al, 2003 ).…”

Section: Plasma Membrane-associated Scaffolding Proteins That Regulatmentioning

confidence: 99%

Scaffold Proteins Regulating Extracellular Regulated Kinase Function in Cardiac Hypertrophy and Disease

Liang

Sheikh

2016

Front. Pharmacol.

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The mitogen activated protein kinase (MAPK)-extracellular regulated kinase 1/2 (ERK1/2) pathway is a central downstream signaling pathway that is activated in cardiac muscle cells during mechanical and agonist-mediated hypertrophy. Studies in genetic mouse models deficient in ERK-associated MAPK components pathway have further reinforced a direct role for this pathway in stress-induced cardiac hypertrophy and disease. However, more recent studies have highlighted that these signaling pathways may exert their regulatory functions in a more compartmentalized manner in cardiac muscle. Emerging data has uncovered specific MAPK scaffolding proteins that tether MAPK/ERK signaling specifically at the sarcomere and plasma membrane in cardiac muscle and show that deficiencies in these scaffolding proteins alter ERK activity and phosphorylation, which are then critical in altering the cardiac myocyte response to stress-induced hypertrophy and disease progression. In this review, we provide insights on ERK-associated scaffolding proteins regulating cardiac myofilament function and their impact on cardiac hypertrophy and disease.

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Regulation of cardiac melusin gene expression by hypertrophic stimuli in the rat

Abstract: Multiple hypertrophic stimuli regulate melusin expression predominately in the atria, which may represent a necessary initial step in early adaptive remodelling processes.

Cited by 7 publications

References 58 publications

Effects of pericardiectomy on training- and myocardial infarction-induced left ventricular hypertrophy, chamber dimensions and gene expression

Effects of pericardiectomy on training- and myocardial infarction-induced left ventricular hypertrophy, chamber dimensions and gene expression

TSC-22 up-regulates collagen 3a1 gene expression in the rat heart

Scaffold Proteins Regulating Extracellular Regulated Kinase Function in Cardiac Hypertrophy and Disease

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