Junction Of Muscle Research Articles

Cross-disease comparison of amyotrophic lateral sclerosis and spinal muscular atrophy reveals conservation of selective vulnerability but differential neuromuscular junction pathology.

Neuromuscular junctions are primary pathological targets in the lethal motor neuron diseases spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS). Synaptic pathology and denervation of target muscle fibers has been reported prior to the appearance of clinical symptoms in mouse models of both diseases, suggesting that neuromuscular junctions are highly vulnerable from the very early stages, and are a key target for therapeutic intervention. Here we examined neuromuscular pathology longitudinally in three clinically relevant muscle groups in mouse models of ALS and SMA in order to assess their relative vulnerabilities. We show for the first time that neuromuscular junctions of the extraocular muscles (responsible for the control of eye movement) were resistant to degeneration in endstage SMA mice, as well as in late symptomatic ALS mice. Tongue muscle neuromuscular junctions were also spared in both animal models. Conversely, neuromuscular junctions of the lumbrical muscles of the hind‐paw were vulnerable in both SMA and ALS, with a loss of neuronal innervation and shrinkage of motor endplates in both diseases. Thus, the pattern of selective vulnerability was conserved across these two models of motor neuron disease. However, the first evidence of neuromuscular pathology occurred at different timepoints of disease progression, with much earlier evidence of presynaptic involvement in ALS, progressing to changes on the postsynaptic side. Conversely, in SMA changes appeared concomitantly at the neuromuscular junction, suggesting that mechanisms of neuromuscular disruption are distinct in these diseases. J. Comp. Neurol. 524:1424–1442, 2016. © 2015 The Authors The Journal of Comparative Neurology Published by Wiley Periodicals, Inc.

Commentary: A Hypothesis for Examining Skeletal Muscle Biopsy-Derived Sarcolemmal nNOSμ as Surrogate for Enteric nNOSα Function

Commentary: A Hypothesis for Examining Skeletal Muscle Biopsy-Derived Sarcolemmal nNOSμ as Surrogate for Enteric nNOSα Function

Aging Drosophila melanogaster display altered pre- and postsynaptic ultrastructure at adult neuromuscular junctions.

Although age-related changes in synaptic plasticity are an important focus within neuroscience, little is known about ultrastructural changes of synaptic morphology during aging. Here we report how aging affects synaptic ultrastructure by using fluorescence and electron microscopy at the adult Drosophila neuromuscular junction (NMJ) of ventral abdominal muscles. Mainly four striking morphological changes of aging NMJs were revealed. 1) Bouton size increases with proportionally rising number of active zones (AZs). 2) Synaptic vesicle density at AZs is increased in old flies. 3) Late endosomes, cisternae, and multivesicular bodies accumulate in the presynaptic terminal, and vesicles accumulate between membranes of the terminal bouton and the subsynaptic reticulum. 4) The electron-dense pre- and postsynaptic apposition is expanded in aging NMJs, which is accompanied by an expansion of the postsynaptic glutamate receptor fields. These findings suggest that aging is possibly accompanied by impaired synaptic vesicle release and recycling and a potentially compensatory expansion of AZs and postsynaptic densities.

Ultrasound Imaging of Torn Soleus Muscle

Figure 1. In comparison with the normal side, the left calf appeared markedly swollen, without noticeable ecchymosis. A 51-year-old man was referred for ultrasound (US) examination because of persistent left calf swelling for 3 months. The swelling developed abruptly after he had stumbled against a stone, sustaining an inversion injury to his ankle. He described calf pain and swelling but no ecchymosis. Three months after injury, active and passive range of motion of the ankle and toes were not limited, including ankle plantar flexion and toe flexion. Skin color and sensation also appeared normal over the swollen area (Figure 1). US imaging revealed a hyperechoic, homogeneous mass originating beneath the mid-portion of the Achilles tendon and ending at the posterior proximal tibia, with an intact distal musculotendinous junction of the medial gastrocnemius muscle (Supplemental Video and Figure 2A). The mass was observed to occupy the space between both heads of the gastrocnemius and deep plantar flexors (tibialis posterior, flexor digitorum profoundus and flexor hallucis longus), with overlying anechoic fluid (Supplemental Video and Figure 2B). The patient was eventually diagnosed with tear of the soleus muscle and an organized hematoma. The soleus muscle, originating from the fibula and medial border of the tibia, merges with the gastrocnemius muscle, forming the Achilles tendon and attaching on the calcaneus. Tear of the medial head of the gastrocnemius muscle at the musculotendinous junction (ie, “tennis leg”) is the more common calf muscle tear, and is typically caused by abrupt extension of the knee and simultaneous forced dorsiflexion of the ankle [1,2]. In this patient, there had been a severe ankle sprain with simultaneous knee buckling. As such, although his gastrocnemius muscle had been protected from overload, the soleus muscle had become vulnerable to the twisting force. In addition, we conclude that the lack of ecchymosis could be attributed to the intact

Tendinous Muscle Insertions (Scleromuscular Junctions of the Recti Muscles) in Patients with Ocular Alignment Problems

The purpose of this study was to prove the hypothesis whether the scleromuscular junction of extraocular recti muscle is tendinous. Muscle samples of the 41 extraocular recti muscles of 33 patients and 4 muscle-/eye-matched samples from 2 postmortem eyes, were processed for light/electron microscopy and immunohistochemistry with antibodies against desmin, smooth-muscle actin and muscle regulating proteins like myf3 and myf4 (myogenin), tenascin C and for 8 samples against collagens I to IV. Histological examination of the muscle samples confirmed a thick collagen-structured tissue, specific for muscle tendon; without appearance of muscle tissue. This was confirmed by immunohistochemistry with antibodies against desmin, smooth-muscle actin, myf3 and myf4 (myogenin) and for eight samples with collagens I to IV. Anti-tenascin C marker was only strongly positive in the connective tissue of the blood vessel walls. Electron microscopy demonstrated collagen bundles composed of parallel oriented fibrils with a moderate amount of ground substance. The absence of contractile fibers at the sclerotendinous junction is an entirely normal finding in humans and cannot be related to ocular alignment pathogenesis.

Skeletal muscle triad junction ultrastructure by Focused-Ion-Beam milling of muscle and Cryo-Electron Tomography.

Cryo-electron tomography (cryo-ET) has emerged as perhaps the only practical technique for revealing nanometer-level three-dimensional structural details of subcellular macromolecular complexes in their native context, inside the cell. As currently practiced, the specimen should be 0.1-0.2 microns in thickness to achieve optimal resolution. Thus, application of cryo-ET to intact frozen (vitreous) tissues, such as skeletal muscle, requires that they be sectioned. Cryo-ultramicrotomy is notoriously difficult and artifact-prone when applied to frozen cells and tissue, but a new technique, focused ion beam milling (cryo-FIB), shows great promise for “thinning” frozen biological specimens. Here we describe our initial results in applying cryo-FIB and cryo-ET to triad junctions of skeletal muscle.

Cadaver study of the topography of the musculotendinous junction of the finger extensor muscles: applicability to tendon rupture following closed wrist trauma.

Rupture of the extensor pollicis longus (EPL) tendon in the wrist is a delayed complication that can occur after wrist injury. Several etiology-related hypotheses have been made to explain these ruptures. The one most commonly accepted is necrosis at the musculotendinous junction of the EPL, which is compressed between the extensor retinaculum and dorsal aspect of the radius. To confirm this hypothesis, we performed an anatomical study to show the close relationship between the extensor retinaculum and the musculotendinous junction of the EPL muscle. We calculated the distance between the musculotendinous junction of the various finger extensor muscles and the proximal edge of the extensor retinaculum. We were able to show that this junction is located under the extensor retinaculum for the extensor indicis (EI) and EPL muscles, but the latter is in the third extensor compartment, which is a tight, confined space. Any pressure increase in this space following trauma, for example, can bring about compartment syndrome at this musculotendinous junction, which some authors have found to be poorly vascularized.

Effects of aging and maternal protein restriction on the muscle fibers morphology and neuromuscular junctions of rats after nutritional recovery

Changes in the nutritional status of mothers may predispose their offspring to neuromuscular disorders in the long term. This study evaluated the effects of maternal protein restriction during pregnancy and lactation on the muscle fibers and neuromuscular junctions (NMJs) of the soleus muscle in the offspring of rats at 365 days of age that had undergone nutritional recovery. Wistar rats were divided into two groups: control (CG) – the offspring of mothers fed a normal protein diet (17%) and restricted (RG) – offspring of mothers fed a low protein diet (6%). After lactation, the male pups received standard chow ad libitum. At 365 days, samples of soleus muscle were collected for muscle fiber analysis (HE staining, NADH-TR reaction and ultrastructure), intramuscular collagen quantification (picrosirius red staining) and NMJs analysis (non-specific esterase technique). The cross-sectional area of type I fibers was reduced by 20% and type IIa fibers by 5% while type IIb fibers increased by 5% in the RG compared to the CG. The percentage of intramuscular collagen was 19% lower in the RG. Disorganization of the myofibrils and Z line was observed, with the presence of clusters of mitochondria in both groups. Regarding the NMJs, in the RG there was a reduction of 10% in the area and 17% in the small diameter and an increase of 7% in the large diameter. The results indicate that the effects of maternal protein restriction on muscle fibers and NMJs seem to be long-lasting and irreversible.

Simulation Methods and Validation Criteria for Modeling Cardiac Ventricular Electrophysiology.

We describe a sequence of methods to produce a partial differential equation model of the electrical activation of the ventricles. In our framework, we incorporate the anatomy and cardiac microstructure obtained from magnetic resonance imaging and diffusion tensor imaging of a New Zealand White rabbit, the Purkinje structure and the Purkinje-muscle junctions, and an electrophysiologically accurate model of the ventricular myocytes and tissue, which includes transmural and apex-to-base gradients of action potential characteristics. We solve the electrophysiology governing equations using the finite element method and compute both a 6-lead precordial electrocardiogram (ECG) and the activation wavefronts over time. We are particularly concerned with the validation of the various methods used in our model and, in this regard, propose a series of validation criteria that we consider essential. These include producing a physiologically accurate ECG, a correct ventricular activation sequence, and the inducibility of ventricular fibrillation. Among other components, we conclude that a Purkinje geometry with a high density of Purkinje muscle junctions covering the right and left ventricular endocardial surfaces as well as transmural and apex-to-base gradients in action potential characteristics are necessary to produce ECGs and time activation plots that agree with physiological observations.

Effect of resistance training on neuromuscular junctions of young and aged muscles featuring different recruitment patterns

To examine the effects of aging on neuromuscular adaptations to resistance training (i.e., weight lifting), young (9 months of age) and aged (20 months of age) male rats either participated in a 7-week ladder climbing protocol with additional weight attached to their tails or served as controls (n = 10/group). At the conclusion, rats were euthanized and hindlimb muscles were quickly removed and frozen for later analysis. Longitudinal sections of the soleus and plantaris muscles were collected, and pre- and postsynaptic features of neuromuscular junctions (NMJs) were visualized with immunofluorescence staining procedures. Cross-sections of the same muscles were histochemically stained to determine myofiber profiles (fiber type and size). Statistical analysis was by two-way ANOVA (main effects of age and treatment) with significance set at P ≤ 0.05. Results revealed that training-induced remodeling of NMJs was evident only at the postsynaptic endplate region of soleus fast-twitch myofibers. In contrast, aging was associated with pre- and postsynaptic remodeling in fast- and slow-twitch myofibers of the plantaris. Although both the soleus and the plantaris muscles failed to display either training or aging-related alterations in myofiber size, aged plantaris muscles exhibited an increased expression of type I (slow-twitch) myofibers in conjunction with a reduced percentage of type II (fast-twitch) myofibers, suggesting early stages of sarcopenia. These data demonstrate the high degree of specificity of synaptic modifications made in response to exercise and aging and that the sparsely recruited plantaris is more vulnerable to the effects of aging than the more frequently recruited soleus muscle.

Synaptic bouton properties are tuned to best fit the prevailing firing pattern.

The morphology of presynaptic specializations can vary greatly ranging from classical single-release-site boutons in the central nervous system to boutons of various sizes harboring multiple vesicle release sites. Multi-release-site boutons can be found in several neural contexts, for example at the neuromuscular junction (NMJ) of body wall muscles of Drosophila larvae. These NMJs are built by two motor neurons forming two types of glutamatergic multi-release-site boutons with two typical diameters. However, it is unknown why these distinct nerve terminal configurations are used on the same postsynaptic muscle fiber. To systematically dissect the biophysical properties of these boutons we developed a full three-dimensional model of such boutons, their release sites and transmitter-harboring vesicles and analyzed the local vesicle dynamics of various configurations during stimulation. Here we show that the rate of transmission of a bouton is primarily limited by diffusion-based vesicle movements and that the probability of vesicle release and the size of a bouton affect bouton-performance in distinct temporal domains allowing for an optimal transmission of the neural signals at different time scales. A comparison of our in silico simulations with in vivo recordings of the natural motor pattern of both neurons revealed that the bouton properties resemble a well-tuned cooperation of the parameters release probability and bouton size, enabling a reliable transmission of the prevailing firing-pattern at diffusion-limited boutons. Our findings indicate that the prevailing firing-pattern of a neuron may determine the physiological and morphological parameters required for its synaptic terminals.

Proteomic analysis of laser capture microscopy purified myotendinous junction regions from muscle sections.

The myotendinous junction is a specialized structure of the muscle fibre enriched in mechanosensing complexes, including costameric proteins and core elements of the z-disc. Here, laser capture microdissection was applied to purify membrane regions from the myotendinous junctions of mouse skeletal muscles, which were then processed for proteomic analysis. Sarcolemma sections from the longitudinal axis of the muscle fibre were used as control for the specificity of the junctional preparation. Gene ontology term analysis of the combined lists indicated a statistically significant enrichment in membrane-associated proteins. The myotendinous junction preparation contained previously uncharacterized proteins, a number of z-disc costameric ligands (e.g., actinins, capZ, αB cristallin, filamin C, cypher, calsarcin, desmin, FHL1, telethonin, nebulin, titin and an enigma-like protein) and other proposed players of sarcomeric stretch sensing and signalling, such as myotilin and the three myomesin homologs. A subset were confirmed by immunofluorescence analysis as enriched at the myotendinous junction, suggesting that laser capture microdissection from muscle sections is a valid approach to identify novel myotendinous junction players potentially involved in mechanotransduction pathways.

Importance of gradients in membrane properties and electrical coupling in sinoatrial node pacing.

The sinoatrial node (SAN) is heterogeneous in terms of cell size, ion channels, current densities, connexins and electrical coupling. For example, Nav1.5 (responsible for I Na) and Cx43 (responsible for electrical coupling) are absent from the centre of the SAN (normally the leading pacemaker site), but present in the periphery (at SAN-atrial muscle junction). To test whether the heterogeneity is important for the functioning of the SAN, one- and two-dimensional models of the SAN and surrounding atrial muscle were created. Normal functioning of the SAN (in terms of cycle length, position of leading pacemaker site, conduction times, activation and repolarization sequences and space constants) was observed when, from the centre to the periphery, (i) cell characteristics (cell size and ionic current densities) were changed in a gradient fashion from a central-type (lacking I Na) to a peripheral-type (possessing I Na) and (ii) coupling conductance was increased in a gradient fashion. We conclude that the heterogeneous nature of the node is important for its normal functioning. The presence of Nav1.5 and Cx43 in the periphery may be essential for the node to be able to drive the atrial muscle: Nav1.5 provides the necessary depolarizing current and Cx43 delivers it to the atrial muscle.

A model for creating a single stretch injury in murine biarticular muscle

BackgroundWe developed a single stretch injury model to create damage near the musculotendinous junction (MTJ) of the gastrocnemius muscle in mice. Our hypothesis was that magnitude of muscle injury could be controlled by stepped shortening of the Achilles tendon (AT) prior to a lengthening contraction. Increased shortening would result in a greater isometric torque deficit and morphological damage 24 hours post-injury.MethodsSixteen mice were randomly assigned to sham or injury predicated on stepped increases in AT shortening. The AT was exposed and placed in a customized stainless steel roller-clamp system to achieve a specific level of shortening; 0 mm (resting length), 0.7 mm or 1.4 mm. Plantar flexors were stimulated to tetany with a needle electrode and then actively lengthened at 450°/sec from neutral to 75° of dorsiflexion. Passive and isometric torques were measured pre- and immediately post-injury. Isometric torque was measured again 24 h post-injury. Peak isokinetic torque was recorded during eccentric injury.ResultsInjury resulted in decreased passive and immediate absolute isometric torque only when induced with AT shortening. The percentage of pre-injury isometric torque was significantly lower in the AT shortened groups immediately and 24 h post-injury, but was unaffected by the level of shortening. Relative isometric torque deficits were noted in the 0 mm group only 24 h post-injury. Peak isokinetic torque during injury was similar in all groups. Histological evaluation 24 h post-injury revealed increased morphological damage near the MTJ in the AT shortened groups.ConclusionSingle stretch with AT shortening created morphological damage near the MTJ and isometric torque deficits immediately and 24 h post-injury, but the magnitude of damage could not be titrated with stepped increases in AT shortening. This model provides an opportunity to utilize transgenic mice in order to elucidate inflammatory mediators that promote regeneration and inhibit fibrosis in order to optimize therapeutic interventions for complete functional recovery.

Tissue‐Engineered Cellular Neotendinous Constructs for Chronic Hernia Repair in a Rat (LB34)

Objective: Over 200,000 incisional hernia repairs are performed each year in the United States at a cost of over $2.5 billion. Currently, hernias are repaired using either alloplastic meshes or soft tissue-derived prostheses; however, recurrence rates remain 10-20% after primary repair and as high as 60% after repair of recurrent hernias. We have developed cellular neotendinous constructs (CNTs), scaffoldless 3-D tissue-engineered prostheses for hernia repair. Our CNTs integrate into the native muscle of the abdominal wall and allow infiltration of host cells, which may prevent junction failure and chronic prosthesis attenuation, the primary causes of hernia recurrence. The purpose of this preliminary study was to assess the potential of our CNTs as improved tissue prostheses for chronic hernia repair in a rat model. Methods: Bone marrow stromal cells were isolated from Fischer 344 rats and used to produce the CNT constructs. Two-centimeter incisional hernias were created along the abdominal midline in ten Fischer 344 rats and left unrepaired for one month. A single CNT was used to close each defect site and 56 days were allowed for recovery. Biomechanical analyses were performed using a novel burst pressure test. Results: After 56 days in vivo, our CNTs fully repaired seven of the ten hernias. When subjected to pressure testing, four of the repair sites resisted substantial pressures, bursting at a mean of 65 kPa, 57% of native abdominal wall burst pressure. Histological analysis of the repair sites indicated the formation of robust CNT-host muscle junctions. Figure 1. A single CNT (A) was implanted into each chronic hernia site (B&C). After 56 days, seven of the ten hernias had been closed (D). Figure 2. Of the seven repaired abdominal walls, four were able to withstand significant hydraulic pressure, bursting at 56% of the mean control pressure. Error bars indicate standard error. Conclusions: These data indicate that our CNTs warrant further study as tissue prostheses for ventral hernia repair. In future work, we will develop more durable CNTs which we hypothesize will provide improved repairs with biomechanical properties approaching those of native abdominal wall.

인체 족저굴곡근의 근력과 아킬레스 건의 경도, 기능적 능력 간 상관관계 분석

Tendon elasticity is an important factor affecting muscle function and thus human movements. It has been reported that the mechanical properties of tendon are adaptable to external loading condition. Based on the adaptability of muscle and tendon to external loading conditions, one can assume that there might be an optimum ratio between muscle strength and tendon stiffness. The present study aimed to investigate whether there is correlation between plantar flexor muscle strength and stiffness of the achilles tendon (AT). Twenty two male subjects (age: 23.2±1.5 yrs, height: 175.5±6.2 cm, weight: 75.4±9.8 kg) performed max- imum voluntary isometric plantarflexion on a custom-built dynamometer and muscle-tendon junction of the medial gastrocnemius muscle was simultaneously monitored using a real-time ultrasound imaging machine. The averages of muscle force and tendon stiffness were 366.38±79.37 N, 35.34±10.42 N/mm, respectively. Significant positive correlation was observed between muscle strength and tendon stiffness (r=0.8507), indicating that the muscle force is proportional to tendon stiffness. The results might have been used in computational modeling and criterion of training progress level in the fields of training and rehabilitation

A Comparative Study of N-glycolylneuraminic Acid (Neu5Gc) and Cytotoxic T Cell (CT) Carbohydrate Expression in Normal and Dystrophin-Deficient Dog and Human Skeletal Muscle

The expression of N-glycolylneuraminic acid (Neu5Gc) and the cytotoxic T cell (CT) carbohydrate can impact the severity of muscular dystrophy arising from the loss of dystrophin in mdx mice. Here, we describe the expression of these two glycans in skeletal muscles of dogs and humans with or without dystrophin-deficiency. Neu5Gc expression was highly reduced (>95%) in muscle from normal golden retriever crosses (GR, n = 3) and from golden retriever with muscular dystrophy (GRMD, n = 5) dogs at multiple ages (3, 6 and 13 months) when compared to mouse muscle, however, overall sialic acid expression in GR and GRMD muscles remained high at all ages. Neu5Gc was expressed on only a minority of GRMD satellite cells, CD8+ T lymphocytes and macrophages. Human muscle from normal (no evident disease, n = 3), Becker (BMD, n = 3) and Duchenne (DMD, n = 3) muscular dystrophy individuals had absent to very low Neu5Gc staining, but some punctate intracellular muscle staining was present in BMD and DMD muscles. The CT carbohydrate was localized to the neuromuscular junction in GR muscle, while GRMD muscles had increased expression on a subset of myofibers and macrophages. In humans, the CT carbohydrate was ectopically expressed on the sarcolemmal membrane of some BMD muscles, but not normal human or DMD muscles. These data are consistent with the notion that altered Neu5Gc and CT carbohydrate expression may modify disease severity resulting from dystrophin deficiency in dogs and humans.

The interaction between tropomyosin-related kinase B receptors and serine kinases modulates acetylcholine release in adult neuromuscular junctions

We conducted an electrophysiological study of the functional link between the tropomyosin-related kinase B (trkB) receptor signaling mechanism and serine-threonine kinases, both protein kinase C (PKC) and protein kinase A (PKA). We describe their coordinated role in transmitter release at the neuromuscular junction (NMJ) of the Levator auris longus muscle of the adult mouse. The trkB receptor normally seems to be coupled to stimulate ACh release because inhibiting the trkB receptor with K-252a results in a significant reduction in the size of EPPs. We found that the intracellular PKC pathway can operate as in basal conditions (to potentiate ACh release) without the involvement of the trkB receptor function, although the trkB pathway needs an operative PKC pathway if it is to couple to the release mechanism and potentiate it. To actively stimulate PKA (which also results in ACh release potentiation), the operativity of trkB is a necessary condition, and one effect of trkB may be PKA stimulation.

Chapter Three - New Insights into the Roles of Xin Repeat-Containing Proteins in Cardiac Development, Function, and Disease

Since the discovery of Xin repeat-containing proteins in 1996, the importance of Xin proteins in muscle development, function, regeneration, and disease has been continuously implicated. Most Xin proteins are localized to myotendinous junctions of the skeletal muscle and also to intercalated discs (ICDs) of the heart. The Xin gene is only found in vertebrates, which are characterized by a true chambered heart. This suggests that the evolutionary origin of the Xin gene may have played a key role in vertebrate origins. Diverse vertebrates including mammals possess two paralogous genes, Xinα (or Xirp1) and Xinβ (or Xirp2), and this review focuses on the role of their encoded proteins in cardiac muscles. Complete loss of mouse Xinβ (mXinβ) results in the failure of forming ICD, severe growth retardation, and early postnatal lethality. Deletion of mouse Xinα (mXinα) leads to late-onset cardiomyopathy with conduction defects. Molecular studies have identified three classes of mXinα-interacting proteins: catenins, actin regulators/modulators, and ion-channel subunits. Thus, mXinα acts as a scaffolding protein modulating the N-cadherin-mediated adhesion and ion-channel surface expression. Xin expression is significantly upregulated in early stages of stressed hearts, whereas Xin expression is downregulated in failing hearts from various human cardiomyopathies. Thus, mutations in these Xin loci may lead to diverse cardiomyopathies and heart failure.

A novel artificial nerve graft for repairing long-distance sciatic nerve defects: a self-assembling peptide nanofiber scaffold-containing poly(lactic-co-glycolic acid) conduit.

In this study, we developed a novel artificial nerve graft termed self-assembling peptide nanofiber scaffold (SAPNS)-containing poly(lactic-co-glycolic acid) (PLGA) conduit (SPC) and used it to bridge a 10-mm-long sciatic nerve defect in the rat. Retrograde tracing, behavioral testing and histomorphometric analyses showed that compared with the empty PLGA conduit implantation group, the SPC implantation group had a larger number of growing and extending axons, a markedly increased diameter of regenerated axons and a greater thickness of the myelin sheath in the conduit. Furthermore, there was an increase in the size of the neuromuscular junction and myofiber diameter in the target muscle. These findings suggest that the novel artificial SPC nerve graft can promote axonal regeneration and remyelination in the transected peripheral nerve and can be used for repairing peripheral nerve injury.