Human essential myosin light chain isoforms revealed distinct myosin binding, sarcomeric sorting, and inotropic activity

Petzhold, Daria; Lossie, Janine; Keller, Sandro; Werner, Sascha; Haase, Hannelore; Morano, Ingo

doi:10.1093/cvr/cvr026

Cited by 18 publications

(17 citation statements)

References 26 publications

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“…Skinned cardiac muscle fibers from these patients exhibit enhanced Ca 2+ sensitivity, accelerated shortening velocity, and faster tension development (388, 390), similar to skinned ventricular fibers from transgenic mice overexpressing Myl4 (144). Consistently, overexpression of human MYL4 in rat hearts subjected to aortocaval shunt operation resulted in attenuation of heart failure (3), while replacement of Myl3 by human MYL4 in adult rat cardiomyocytes led to accelerated contractility kinetics without altering Ca 2+ signaling (438). Thus, upregulation of MYL4 may serve as a compensatory mechanism to enhance cardiac contractility in patients with different types of cardiomyopathy possibly by reducing the binding affinity between ELC and actin therefore enabling faster actomyosin contractions.…”

Section: Myosinmentioning

confidence: 90%

“…2B) (408,434,541,559). MYL3 and MYL4 share considerable homology (80.1% identity and 90.3% similarity); however, they exhibit distinct affinities to myosin and actin with MYL3 binding more efficiently to actin and MYL4 to MyHC (438, 439). MYL4 is upregulated in the ventricles of patients with tetralogy or trilogy of Fallot, double-outlet right ventricle disease, infundibular pulmonary stenosis, and hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM) (30, 388, 390, 499).…”

Section: Myosinmentioning

confidence: 99%

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Thick Filament Protein Network, Functions, and Disease Association

Wang

Geist

Grogan

et al. 2018

Comprehensive Physiology

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Sarcomeres consist of highly ordered arrays of thick myosin and thin actin filaments along with accessory proteins. Thick filaments occupy the center of sarcomeres where they partially overlap with thin filaments. The sliding of thick filaments past thin filaments is a highly regulated process that occurs in an ATP-dependent manner driving muscle contraction. In addition to myosin that makes up the backbone of the thick filament, four other proteins which are intimately bound to the thick filament, myosin binding protein-C, titin, myomesin, and obscurin play important structural and regulatory roles. Consistent with this, mutations in the respective genes have been associated with idiopathic and congenital forms of skeletal and cardiac myopathies. In this review, we aim to summarize our current knowledge on the molecular structure, subcellular localization, interacting partners, function, modulation via posttranslational modifications, and disease involvement of these five major proteins that comprise the thick filament of striated muscle cells. © 2018 American Physiological Society. Compr Physiol 8:631-709, 2018.

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Section: Myosinmentioning

confidence: 90%

Section: Myosinmentioning

confidence: 99%

Thick Filament Protein Network, Functions, and Disease Association

Wang

Geist

Grogan

et al. 2018

Comprehensive Physiology

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“…Ventricular cardiomyocytes were isolated from 2-3 month old female and male WT- and ERα-OE mice by a standard enzymatic technique as described before [30]. Briefly, animals were anesthetized with isoflurane, followed by intraperitoneal injection of 8 μg xylazine and 35 μg ketamine.…”

Section: Methodsmentioning

confidence: 99%

Cardiomyocyte-specific Estrogen Receptor Alpha Increases Angiogenesis,Lymphangiogenesis and Reduces Fibrosis in the Female Mouse Heart Post-Myocardial Infarction

et al. 2014

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Experimental studies showed that 17β-estradiol (E2) and activated Estrogen Receptors (ER) protect the heart from ischemic injury. However, the underlying molecular mechanisms are not well understood. To investigate the role of ER-alpha (ERα) in cardiomyocytes in the setting of myocardial ischemia, we generated transgenic mice with cardiomyocyte-specific overexpression of ERα (ERα-OE) and subjected them to Myocardial Infarction (MI). At the basal level, female and male ERα-OE mice showed increased Left Ventricular (LV) mass, LV volume and cardiomyocyte length. Two weeks after MI, LV volume was significantly increased and LV wall thickness decreased in female and male WT-mice and male ERα-OE, but not in female ERα-OE mice. ERα-OE enhanced expression of angiogenesis and lymphangiogenesis markers (Vegf, Lyve-1), and neovascularization in the peri-infarct area in both sexes. However, attenuated level of fibrosis and higher phosphorylation of JNK signaling pathway could be detected only in female ERα-OE after MI. In conclusion, our study indicates that ERα protects female mouse cardiomyocytes from the sequelae of ischemia through induction of neovascularization in a paracrine fashion and impaired fibrosis, which together may contribute to the attenuation of cardiac remodelling.

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“…Ventricular cardiomyocytes were isolated from adult female and male C57BL/6J mice (n=4-5 hearts each; 3-4 months) as described before [29]. Briefly, after cervical dislocation, the hearts were rapidly excised and perfused with a low Ca 2+ , collagenase bicarbonate buffer solution (36°C, pH 7.4) for 10 min.…”

Section: Isolation Of Adult Mouse Ventricular Cardiomyocytes and Cultmentioning

confidence: 99%

Nuclear translocation of the cardiac L-type calcium channel C-terminus is regulated by sex and 17β-estradiol

Mahmoodzadeh

Haase

Sporbert

et al. 2016

Journal of Molecular and Cellular Cardiology

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Human essential myosin light chain isoforms revealed distinct myosin binding, sarcomeric sorting, and inotropic activity

Abstract: Intense myosin binding of hALC-1 provides a mechanism for preferential sarcomeric sorting and Ca(2+)-independent positive inotropic activity.

Cited by 18 publications

References 26 publications

Thick Filament Protein Network, Functions, and Disease Association

Thick Filament Protein Network, Functions, and Disease Association

Cardiomyocyte-specific Estrogen Receptor Alpha Increases Angiogenesis,Lymphangiogenesis and Reduces Fibrosis in the Female Mouse Heart Post-Myocardial Infarction

Nuclear translocation of the cardiac L-type calcium channel C-terminus is regulated by sex and 17β-estradiol

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