Molecular regulation of postsynaptic differentiation at the neuromuscular junction

Madhavan, Raghavan; Peng, H. Benjamin

doi:10.1080/15216540500338739

Cited by 33 publications

(32 citation statements)

References 135 publications

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“…In mature myotubes Met is down-regulated, but some residual expression has been documented in the literature (52). We verified by Western blot that Met is expressed in adult skeletal muscle and that its level increases in the cachectic muscle of tumor bearing C-26 mice.…”

Section: Discussionsupporting

confidence: 49%

Conditional Activation of MET in Differentiated Skeletal Muscle Induces Atrophy

Crepaldi¹,

Bersani²,

Scuoppo³

et al. 2007

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 49%

Conditional Activation of MET in Differentiated Skeletal Muscle Induces Atrophy

Crepaldi¹,

Bersani²,

Scuoppo³

et al. 2007

Journal of Biological Chemistry

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“…Prior to innervation embryonic muscles contain nerve independent or aneural clusters of analysis of acetylcholine receptors (AChRs). Subsequently, motor axons extend upon muscles and induce nerve dependent AChR clusters at the incipient NMJ and disperse non-synaptic AChR clusters (Madhavan and Peng, 2005). The induction of AChR aggregates at the NMJ requires zagrin, a neural specific form of a heparan sulfate proteoglycan that is secreted by the motor axons and is both necessary and sufficient for nerve dependent aggregation of AChR clusters (Godfrey et al, 1984;Ferns and Hall, 1992;Hoch et al, 1994;Gautam et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stability

Saint-Amant

Sprague

Hirata

et al. 2007

Developmental Neurobiology

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The zebrafish ennui mutation was identified from a mutagenesis screen for defects in early behavior. Homozygous ennui embryos swam more slowly than wild-type siblings but normal swimming recovered during larval stages and homozygous mutants survived until adulthood. Electrophysiological recordings from motoneurons and muscles suggested that the motor output of the CNS following mechanosensory stimulation was normal in ennui, but the synaptic currents at the neuromuscular junction were significantly reduced. Analysis of acetylcholine receptors (AChRs) in ennui muscles showed a marked reduction in the size of synaptic clusters and their aberrant localization at the myotome segment borders of fast twitch muscle. Prepatterned, nerve-independent AChR clusters appeared normal in mutant embryos and dispersed upon outgrowth of motor axons onto the muscles. Genetic mosaic analysis showed that ennui is required cell autonomously in muscle fibers for normal synaptic localization of AChRs. Furthermore, exogenous agrin failed to induce AChR aggregation, suggesting that ennui is crucial for agrin function. Finally, motor axons branched more extensively in ennui fast twitch muscles especially in the region of the myotome borders. These results suggest that ennui is important for nerve-dependent AChR clustering and the stability of axon growth.

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“…One possible reason for the lack of long-term success is the micro-environmental role played by axons that innervate the muscle and form NMJs (Sanes and Lichtman, 2001; Madhavan and Peng, 2005; Witzemann, 2006; Wu et al, 2010). In native, healthy muscle tissue innervation is indicated by the formation of a mature post-synaptic apparatus known as the motor end plate (MEP) (Sanes and Lichtman, 2001; Madhavan and Peng, 2005; Witzemann, 2006; Wu et al, 2010). In non-VML injuries to skeletal muscle, re-innervation is achieved when endplates remain present (Frank et al, 1975; Carlson and Faulkner, 1988; Dedkov et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Achieving Acetylcholine Receptor Clustering in Tissue-Engineered Skeletal Muscle Constructs In vitro through a Materials-Directed Agrin Delivery Approach

et al. 2017

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Volumetric muscle loss (VML) can result from trauma, infection, congenital anomalies, or surgery, and produce permanent functional and cosmetic deficits. There are no effective treatment options for VML injuries, and recent advances toward development of muscle constructs lack the ability to achieve innervation necessary for long-term function. We sought to develop a proof-of-concept biomaterial construct that could achieve acetylcholine receptor (AChR) clustering on muscle-derived cells (MDCs) in vitro. The approach consisted of the presentation of neural (Z+) agrin from the surface of microspheres embedded with a fibrin hydrogel to muscle cells (C2C12 cell line or primary rat MDCs). AChR clustering was spatially restricted to areas of cell (C2C12)-microsphere contact when the microspheres were delivered in suspension or when they were incorporated into a thin (2D) fibrin hydrogel. AChR clusters were observed from 16 to 72 h after treatment when Z+ agrin was adsorbed to the microspheres, and for greater than 120 h when agrin was covalently coupled to the microspheres. Little to no AChR clustering was observed when agrin-coated microspheres were delivered from specially designed 3D fibrin constructs. However, cyclic stretch in combination with agrin-presenting microspheres led to dramatic enhancement of AChR clustering in cells cultured on these 3D fibrin constructs, suggesting a synergistic effect between mechanical strain and agrin stimulation of AChR clustering in vitro. These studies highlight a strategy for maintaining a physiological phenotype characterized by motor endplates of muscle cells used in tissue engineering strategies for muscle regeneration. As such, these observations may provide an important first step toward improving function of tissue-engineered constructs for treatment of VML injuries.

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Molecular regulation of postsynaptic differentiation at the neuromuscular junction

Cited by 33 publications

References 135 publications

Conditional Activation of MET in Differentiated Skeletal Muscle Induces Atrophy

Conditional Activation of MET in Differentiated Skeletal Muscle Induces Atrophy

The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stability

Achieving Acetylcholine Receptor Clustering in Tissue-Engineered Skeletal Muscle Constructs In vitro through a Materials-Directed Agrin Delivery Approach

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