Patterns of Expression of the Follistatin and Follistatin‐Like1 Genes During Chicken Heart Development: A Potential Role in Valvulogenesis and Late Heart Muscle Cell Formation

Berg, Gert van den; Somi, Semir; Buffing, Anita A.M.; Moorman, Antoon F.M.; Hoff, Maurice J.B. van den

doi:10.1002/ar.20559

Cited by 19 publications

(10 citation statements)

References 33 publications

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“…Involvement of FSTL1 in cardiovascular tissue regulation has been suggested (20,(27)(28)(29). Its expression in adult heart is induced in response to injurious conditions that promote myocardial hypertrophy and heart failure (21,30,31).…”

Section: Introductionmentioning

confidence: 99%

Expression, characterization, and preliminary X-ray crystallographic analysis of recombinant murine Follistatin-like 1 expressed in Drosophila S2 cells

Xue

et al. 2013

Biosci Trends

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Section: Introductionmentioning

confidence: 99%

Expression, characterization, and preliminary X-ray crystallographic analysis of recombinant murine Follistatin-like 1 expressed in Drosophila S2 cells

Xue

et al. 2013

Biosci Trends

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“…Myostatin is expressed in both fetal and adult ovine hearts, specifically in the cardiomyocytes and Purkinje fibres (Sharma et al 1999; Shyu et al 2005), and is co‐expressed with FSTL‐3 and follistatin in the ventricles, atria and/or valves of developing mice and chicken (Takehara‐Kasamatsu et al 2007; van den Berg et al 2007). Its expression also similarly increases with insult in both cardiac and skeletal muscle (Rodgers & Garikipati, 2008), suggesting that myostatin may additionally influence the growth and development of both tissues.…”

Section: Introductionmentioning

confidence: 99%

Myostatin represses physiological hypertrophy of the heart and excitation–contraction coupling

Rodgers¹,

Interlichia²,

Garikipati³

et al. 2009

The Journal of Physiology

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Although myostatin negatively regulates skeletal muscle growth, its function in heart is virtually unknown. Herein we demonstrate that it inhibits basal and IGF-stimulated proliferation and differentiation and also modulates cardiac excitation-contraction (EC) coupling. Loss of myostatin induced eccentric hypertrophy and enhanced cardiac responsiveness to β-adrenergic stimulation in vivo. This was due to myostatin null ventricular myocytes having larger [Ca 2+ ] i transients and contractions and responding more strongly to β-adrenergic stimulation than wild-type cells. Enhanced cardiac output and β-adrenergic responsiveness of myostatin null mice was therefore due to increased SR Ca 2+ release during EC coupling and to physiological hypertrophy, but not to enhanced myofilament function as determined by simultaneous measurement of force and ATPase activity. Our studies support the novel concept that myostatin is a repressor of physiological cardiac muscle growth and function. Thus, the controlled inhibition of myostatin action could potentially help repair damaged cardiac muscle by inducing physiological hypertrophy.

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“…Follistatin binds to activins, which are members of the TGFβ family implicated in diverse biological processes including cell proliferation, cell differentiation, fibrosis and the development of atherosclerosis [32,33]. Both FST and FSTL-1 are expressed in normal heart [34] and markedly increased in heart failure [35]. Since overexpression of FSTL-1 attenuates cardiac myocyte apoptosis induced by hypoxia/reperfusion injury [36], up-regulation of FSTL-1 induced by ß 1 AR expression might represent a compensation mechanism elicited by damaged cardiac myocytes.…”

Section: Discussionmentioning

confidence: 99%

β1-Adrenergic receptor vs adenylyl cyclase 6 expression in cardiac myocytes: Differences in transgene localization and intracellular signaling

Gao

Tang

Miyanohara

et al. 2010

Cellular Signalling

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Adenylyl cyclase type 6 (AC6) and the ß 1 adrenergic receptor (ß 1 AR) are pivotal proteins in transmembrane ßAR-signaling in cardiac myocytes. Increased expression of AC6 has beneficial effects on the heart, but increased ß 1 AR expression has marked deleterious effects. Why do these two elements of the ßAR pathway have such different effects? Using adenovirus-mediated gene transfer of the two transgenes in neonatal rat cardiac myocytes, we assessed cellular distribution and performed selected biochemical assays. ß 1 AR was found predominantly in the plasma membrane. In contrast, AC6 was found in the plasma membrane but also was associated with the nuclear envelope, sarcoplasmic reticulum, mitochondria, and cytoplasm. Increased ß 1 AR, but not AC6, increased follistatin expression, p38 phosphorylation, phosphatidylserine translocation to the PM, and apoptosis. In contrast, increased AC6, but not ß 1 AR, inhibited PHLPP2 activity, activated PI3K and Akt, and increased p70S6 kinase phosphorylation and Bcl-2 expression; apoptosis was unchanged. The distribution of AC6 to multiple cellular compartments appears to enable interactions with other proteins (eg, PHLPP2) and activates cardioprotective signaling (PI3K/Akt). In contrast, ß 1 AR, confined to the plasma membrane, increased phosphatidylserine translocation and apoptosis. These data provide a potential underlying mechanism for the beneficial vs deleterious effects of these two related ßAR-signaling elements.

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Patterns of Expression of the Follistatin and Follistatin‐Like1 Genes During Chicken Heart Development: A Potential Role in Valvulogenesis and Late Heart Muscle Cell Formation

Cited by 19 publications

References 33 publications

Expression, characterization, and preliminary X-ray crystallographic analysis of recombinant murine Follistatin-like 1 expressed in Drosophila S2 cells

Expression, characterization, and preliminary X-ray crystallographic analysis of recombinant murine Follistatin-like 1 expressed in Drosophila S2 cells

Myostatin represses physiological hypertrophy of the heart and excitation–contraction coupling

β1-Adrenergic receptor vs adenylyl cyclase 6 expression in cardiac myocytes: Differences in transgene localization and intracellular signaling

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