MuRF1 is a muscle fiber-type II associated factor and together with MuRF2 regulates type-II fiber trophicity and maintenance

Moriscot, Anselmo Sigari; Baptista, Igor L.; Bogomolovas, Julius; Witt, Christian; Hirner, Stephanie; Granzier, Henk; Labeit, Siegfried

doi:10.1016/j.jsb.2010.02.001

Cited by 76 publications

(86 citation statements)

References 36 publications

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“…This reduction occurs selectively in type II fibers, consistent with the results of others (32). These changes are associated with high levels of NF-kB activity in ALI muscles ( Figures 4E and 4F), which others have shown to be important in promoting muscle wasting associated with tumor cachexia (29) or denervation (27).…”

Section: Discussionsupporting

confidence: 89%

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

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D’Alessio²,

Johnston³

et al. 2012

Am J Respir Crit Care Med

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Rationale: Acute lung injury (ALI) is a debilitating condition associated with severe skeletal muscle weakness that persists in humans long after lung injury has resolved. The molecular mechanisms underlying this condition are unknown. Objectives: To identify the muscle-specific molecular mechanisms responsible for muscle wasting in a mouse model of ALI. Methods: Changes in skeletal muscle weight, fiber size, in vivo contractile performance, and expression of mRNAs and proteins encoding muscle atrophy-associated genes for muscle ring finger-1 (MuRF1) and atrogin1 were measured. Genetic inactivation of MuRF1 or electroporationmediated transduction of miRNA-based short hairpin RNAs targeting either MuRF1 or atrogin1 were used to identify their role in ALIassociated skeletal muscle wasting. Measurements and Main Results: Mice with ALI developed profound muscle atrophy and preferential loss of muscle contractile proteins associated with reduced muscle function in vivo. Although mRNA expression of the muscle-specific ubiquitin ligases, MuRF1 and atrogin1, was increased in ALI mice, only MuRF1 protein levels were up-regulated. Consistent with these changes, suppression of MuRF1 by genetic or biochemical approaches prevented muscle fiber atrophy, whereas suppression of atrogin1 expression was without effect. Despite resolution of lung injury and down-regulation of MuRF1 and atrogin1, force generation in ALI mice remained suppressed. Conclusions: These data show that MuRF1 is responsible for mediating muscle atrophy that occurs during the period of active lung injury in ALI mice and that, as in humans, skeletal muscle dysfunction persists despite resolution of lung injury.Keywords: skeletal muscle atrophy; intensive care unit-acquired weakness; critical illness myopathy; muscle atrophy genes; proteasomal-mediated protein degradation Acute lung injury (ALI) is a syndrome characterized by the acute onset of pulmonary infiltrates and respiratory failure often leading to the need for mechanical ventilation (1). Approximately 200,000 people per year develop ALI in the United States, with mortality high at 30-40% (2). A common complication associated with ALI is skeletal muscle weakness. Weakness in these patients results in decreased long-term mobility and functional status. Skeletal muscle weakness is initiated early in the course of ALI, and has been shown to persist in a large percentage of patients for up to 5 years after resolution of lung injury and hospital discharge (3-6). Although multiple factors may contribute to ALI-induced muscle atrophy including reduced nutrition, inactivity caused by bed rest, and systemic inflammation, the etiology of ALI-associated skeletal muscle atrophy remains incompletely understood.Skeletal muscle weakness is a common finding not only among patients with ALI, but also in patients with other critical illnesses. Clinically apparent weakness is present in 20-50% of patients with critical illness and has been shown to be an independent risk factor for mortality in these patients (3,5,7,8)....

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Section: Discussionsupporting

confidence: 89%

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

Files

D’Alessio²,

Johnston³

et al. 2012

Am J Respir Crit Care Med

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“…MYOZ1 is involved in fast and slow twitch fiber switching (Moriscot et al, 2010), which suggests that miR-432 may also be associated with muscle fiber composition in skeletal muscles. We first investigated the effect of miR-432 on myoblast proliferation in the C2C12 cell line.…”

Section: Discussionmentioning

confidence: 99%

“…MuRF1/MuRF2 KO mice exhibited loss of myozenin-1 expression in the tibialis anterior muscle, suggesting that MuRF1/MuRF2 act as regulators of the calcineurin/NFAT pathway. Therefore, MuRF1 and MuRF2 together are required for maintenance of type-II fibers, possibly via regulation of MYOZ (Moriscot et al, 2010). MYOZ1 knockout mice showed augmented exercise abilities as well as elevated slow muscle fiber type ratio in skeletal muscles (Frey et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…It has been suggested that MYOZ1 family members may contribute to the formation and maintenance of Z-discs and may also be involved in cell signaling via binding to calcineurin (Wang et al, 2006;Arola et al, 2007). Furthermore, MYOZ1 may be involved in remodeling and maintenance of type-II fibers via NuRF1 and NuRF2 regulation (Moriscot et al, 2010). MYOZ1 and MYOZ3 are highly expressed in fast twitch muscle fibers, whereas MYOZ2 is highly expressed in cardiac muscle slow twitch fibers (von Nandelstadh et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Targeting of miR-432 to myozenin1 to regulate myoblast proliferation and differentiation

Ren¹,

Liu²,

Zhao³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. MicroRNAs (miRNAs) play important roles in the development and biochemical functions of skeletal muscles. However, targeting of miRNAs to structural genes involved in Z-discs have not been investigated. Here, we describe a highly expressed miRNA, miR-432, in pig embryonic skeletal muscle, which appeared to target myozenin1 (MYOZ1), a protein involved in the muscular sarcomere microstructure. Our results showed that miR-432 is involved in muscle development in the developing pig. In addition, it promoted differentiation of the C2C12 myoblast cell line into myotubes. We also demonstrated that inhibition of miR-432 reduced proliferation of C2C12 cells, suggesting that miR-432 is involved in regulation of myoblast proliferation. Moreover, molecular markers of muscle differentiation and fiber type (Myh7/ slow and Myh4/ fast IIB) showed that miR-432 reduced the differentiation rate of C2C12 cells. These results provide insights into the potential functions of miR-432 as well as its proposed target, MYOZ1, during muscle development. This may lead to applications for further improvements in porcine muscle growth, and may enhance our understanding of complex inherited human muscle disorders.

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“…The muscle fiber length and strength of the 3 parts are similar to those of the biceps brachii; therefore, this is an ideal material for functional reconstruction of the elbow (Atkins et al, 1985;Chomiak & Dungl, 2008). the literature (Moriscot et al, 2010;Goncalves et al, 2012). However, their expression in the donor and recipient muscles after muscle transplantation has not been sufficiently studied.…”

Section: Introductionmentioning

confidence: 99%

Expression of MuRF1 and MAFbx in Donor and Recipient Muscles after Musculocutaneous Nerve Transection and Partial Pectoralis Major Muscle Transfer for Reconstruction of Elbow Flexion in Rats

2015

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. Expression of murf1 and mafbx in donor and recipient muscles after musculocutaneous nerve transection and partial pectoralis major muscle transfer for reconstruction of elbow flexion in rats. Int. J. Morphol., 33(3):975-982, 2015. SUMMARY:The expression of MuRF1 and MAFbx in a denervated muscle has previously been studied. However, the expression of MuRF1 and MAFbx in the recipient and donor muscles after muscle transfer for reconstruction of joint function has not been sufficiently investigated. Forty-two adult Sprague-Dawley rats were divided into 7 groups: normal, 1 w post-, 2 w post-, and 4 w post-musculocutaneous nerve transection; and 1 w post-, 2 w post-, and 4 w post-reconstruction of elbow flexion. Muscle wet weights were assessed, and MuRF1 and MAFbx mRNA expressions were detected by polymerase chain reaction. The length of the oblique part of the pectoralis major of an SD rat is sufficient for suture to the insertion of the biceps brachii tendon. The muscle wet weight and the wet weight retention rate of the biceps brachii continued to decline after musculocutaneous nerve transection and a gradual increase was noted after the oblique part of the pectoralis major was transferred for reconstruction of elbow flexion. The oblique part of the pectoralis major showed a decrease of only 2-6%. The upregulated expression of MuRF1 and MAFbx in the biceps brachii reached a peak 2 w after denervation and 1 w after elbow flexion reconstruction, with an increase of 15% and 4%, respectively. This was followed by downregulation; however, the expression had not normalized at postoperative 4 w. The increased expression of MuRF1 (17%) and MAFbx (1%) in the oblique part of the pectoralis major at postoperative 1 w had decreased to below normal levels at postoperative 4 w. The transfer of the oblique part of the pectoralis major for elbow flexion reconstruction after musculocutaneous nerve transection can downregulate the expression of MuRF1 and MAFbx in the recipient muscle and causes only transient damage to the donor muscle in rats.

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MuRF1 is a muscle fiber-type II associated factor and together with MuRF2 regulates type-II fiber trophicity and maintenance

Cited by 76 publications

References 36 publications

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

Targeting of miR-432 to myozenin1 to regulate myoblast proliferation and differentiation

Expression of MuRF1 and MAFbx in Donor and Recipient Muscles after Musculocutaneous Nerve Transection and Partial Pectoralis Major Muscle Transfer for Reconstruction of Elbow Flexion in Rats

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