Dataset Information

Real-Time Functional Assay of Volumetric Muscle Loss Injured Mouse Masseter Muscles via Nanomembrane Electronics.

ABSTRACT: Skeletal muscle has a remarkable regeneration capacity to recover its structure and function after injury, except for the traumatic loss of critical muscle volume, called volumetric muscle loss (VML). Although many extremity VML models have been conducted, craniofacial VML has not been well-studied due to unavailable in vivo assay tools. Here, this paper reports a wireless, noninvasive nanomembrane system that integrates skin-wearable printed sensors and electronics for real-time, continuous monitoring of VML on craniofacial muscles. The craniofacial VML model, using biopsy punch-induced masseter muscle injury, shows impaired muscle regeneration. To measure the electrophysiology of small and round masseter muscles of active mice during mastication, a wearable nanomembrane system with stretchable graphene sensors that can be laminated to the skin over target muscles is utilized. The noninvasive system provides highly sensitive electromyogram detection on masseter muscles with or without VML injury. Furthermore, it is demonstrated that the wireless sensor can monitor the recovery after transplantation surgery for craniofacial VML. Overall, the presented study shows the enormous potential of the masseter muscle VML injury model and wearable assay tool for the mechanism study and the therapeutic development of craniofacial VML.

SUBMITTER: Kim H

PROVIDER: S-EPMC8425913 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Volumetric muscle loss (VML) injuries represent a majority of military service member casualties and are common in civilian populations following blunt and/or penetrating traumas. Characterized as a skeletal muscle injury with permanent functional impairments, there is currently no standard for rehabilitation, leading to lifelong disability. Toward developing rehabilitative strategies, previous research demonstrates that the remaining muscle after a VML injury lacks similar levels of plasticity or adaptability as healthy, uninjured skeletal muscle. This may be due, in part, to impaired innervation and vascularization of the remaining muscle, as well as disrupted molecular signaling cascades commonly associated with muscle adaptation. The primary objective of this study was to assess the ability of four pharmacological agents with a strong record of modulating muscle contractile and metabolic function to improve functional deficits in a murine model of VML injury. Male C57BL/6 mice underwent a 15% multimuscle VML injury of the posterior hindlimb and were randomized into drug treatment groups (formoterol [FOR], 5-aminoimidazole-4-carboxamide riboside [AICAR], pioglitazone [PIO], or sildenafil [SIL]) or untreated VML group. At the end of 60 days, the injury model was first validated by comparison to age-matched injury-naive mice. Untreated VML mice had 22% less gastrocnemius muscle mass, 36% less peak-isometric torque, and 27% less maximal mitochondrial oxygen consumption rate compared to uninjured mice (p < 0.01). Experimental drug groups were, then, compared to VML untreated, and there was minimal evidence of efficacy for AICAR, PIO, or SIL in improving contractile and metabolic functional outcomes. However, FOR-treated VML mice had 18% greater peak isometric torque (p < 0.01) and permeabilized muscle fibers had 36% greater State III mitochondrial oxygen consumption rate (p < 0.01) compared to VML untreated mice, suggesting an overall improvement in muscle condition. There was minimal evidence that these benefits came from greater mitochondrial biogenesis and/or mitochondrial complex protein content, but could be due to greater enzyme activity levels for complex I and complex II. These findings suggest that FOR treatment is candidate to pair with a rehabilitative approach to maximize functional improvements in VML-injured muscle. Impact statement Volumetric muscle loss (VML) injuries result in deficiencies in strength and mobility, which have a severe impact on patient quality of life. Despite breakthroughs in tissue engineering, there are currently no treatments available that can restore function to the affected limb. Our data show that treatment of VML injuries with clinically available and FDA-approved formoterol (FOR), a beta-agonist, significantly improves strength and metabolism of VML-injured muscle. FOR is therefore a promising candidate for combined therapeutic approaches (i.e., regenerative rehabilitation) such as pairing FOR with structured rehabilitation or cell-seeded biomaterials as it may provide greater functional improvements than either strategy alone.

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Real-Time Functional Assay of Volumetric Muscle Loss Injured Mouse Masseter Muscles via Nanomembrane Electronics.

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