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Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing.

ABSTRACT: Motor unit remodelling involving repeated denervation and re-innervation occurs throughout life. The efficiency of this process declines with age contributing to neuromuscular deficits. This study investigated differentially expressed genes (DEG) in muscle following peroneal nerve crush to model motor unit remodelling in C57BL/6 J mice. Muscle RNA was isolated at 3 days post-crush, RNA libraries were generated using poly-A selection, sequenced and analysed using gene ontology and pathway tools. Three hundred thirty-four DEG were found in quiescent muscle from (26mnth) old compared with (4-6mnth) adult mice and these same DEG were present in muscle from adult mice following nerve crush. Peroneal crush induced 7133 DEG in muscles of adult and 699 DEG in muscles from old mice, although only one DEG (ZCCHC17) was found when directly comparing nerve-crushed muscles from old and adult mice. This analysis revealed key differences in muscle responses which may underlie the diminished ability of old mice to repair following nerve injury.

SUBMITTER: Staunton CA

PROVIDER: S-EPMC8800362 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing

Project description:Motor unit remodelling involving repeated denervation and re-innervation occurs throughout life. The efficiency of this process declines with age contributing to neuromuscular deficits. We investigated differentially expressed genes (DEG) in muscle following peroneal nerve crush to model of motor unit remodelling in C57Bl6 mice. Muscle RNA was isolated at 3 days post-crush, RNA libraries were generated using poly-A selection, sequenced.

2022-01-10 | E-MTAB-10601 | biostudies-arrayexpress

Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing

Project description:Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing

| PRJEB45782 | ENA

Identification of suitable reference genes for gene expression studies in rat skeletal muscle following sciatic nerve crush injury.

Project description:Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) is a molecular biological method used to assess gene expression characterized by high simplicity, effectiveness, specificity and sensitivity. The selection of a suitable reference gene for normalization is critical for the accuracy of quantitative results. Peripheral nerve injury is a common clinical disorder that affects multiple tissues and organs, including peripheral nerves, neurons and the innervated muscles. Numerous genes are differentially expressed in skeletal muscles during muscle denervation and reinnervation following peripheral nerve injury. The identification of a suitable reference gene in innervated muscles following nerve injury may improve the understanding of the alterations in gene expression in the processes of peripheral nerve repair and regeneration. Therefore, in the present study, by using a rat sciatic nerve crush model, the expression levels of various housekeeping genes were examined. In particular, the expression levels of 13 housekeeping genes, including 18S ribosomal RNA, actin β, ankyrin repeat domain 27, cyclophilin A, GAPDH, hypoxanthine phosphoribosyltransferase 1 (HPRT1), mitochondrial ribosomal protein L10, phosphoglycerate kinase 1, RPTOR independent companion of mammalian target of rapamycin complex 2, TATA‑box binding protein, ubiquitin C, UBX domain protein 11 and tyrosine 3‑monooxygenase/tryptophan 5‑monooxygenase activation protein ζ, were investigated in gastrocnemius muscles. The geNorm and NormFinder analyses suggested that the expression level of HPRT1 was particularly stable in gastrocnemius muscles following rat sciatic nerve crush injury. Therefore, HPRT1 may be used as a reference gene for the normalization of gene expression data generated by RT‑qPCR.

| S-EPMC6472138 | biostudies-literature

4-Aminopyridine attenuates muscle atrophy after sciatic nerve crush injury in mice.

Project description:IntroductionWe recently demonstrated the beneficial effects of 4-aminopyridine (4-AP), a potassium channel blocker, in enhancing remyelination and recovery of nerve conduction velocity and motor function after sciatic nerve crush injury in mice. Although muscle atrophy occurs very rapidly after nerve injury, the effect of 4-AP on muscle atrophy and intrinsic muscle contractile function is largely unknown.MethodsMice were assigned to sciatic nerve crush injury and no-injury groups and were followed for 3, 7, and 14 days with/without 4-AP or saline treatment. Morphological, functional, and transcriptional properties of skeletal muscle were assessed.ResultsIn addition to improving in vivo function, 4-AP significantly reduced muscle atrophy with increased muscle fiber diameter and contractile force. Reduced muscle atrophy was associated with attenuated expression of atrophy-related genes and increased expression of proliferating stem cells.DiscussionThese findings provide new insights into the potential therapeutic benefits of 4-AP against nerve injury-induced muscle atrophy and dysfunction. Muscle Nerve 60: 192-201, 2019.

| S-EPMC7397862 | biostudies-literature

Skeletal muscle reprogramming enhances reinnervation after peripheral nerve injury.

Project description:Peripheral Nerve Injuries (PNI) affect more than 20 million Americans and severely impact quality of life by causing long-term disability. The onset of PNI is characterized by nerve degeneration distal to the nerve injury resulting in long periods of skeletal muscle denervation. During this period, muscle fibers atrophy and frequently become incapable of "accepting" innervation because of the slow speed of axon regeneration post injury. We hypothesize that reprogramming the skeletal muscle to an embryonic-like state may preserve its reinnervation capability following PNI. To this end, we generated a mouse model in which NANOG, a pluripotency-associated transcription factor can be expressed locally upon delivery of doxycycline (Dox) in a polymeric vehicle. NANOG expression in the muscle upregulated the percentage of Pax7+ nuclei and expression of eMYHC along with other genes that are involved in muscle development. In a sciatic nerve transection model, NANOG expression led to upregulation of key genes associated with myogenesis, neurogenesis and neuromuscular junction (NMJ) formation, and downregulation of key muscle atrophy genes. Further, NANOG mice demonstrated extensive overlap between synaptic vesicles and NMJ acetylcholine receptors (AChRs) indicating restored innervation. Indeed, NANOG mice showed greater improvement in motor function as compared to wild-type (WT) animals, as evidenced by improved toe-spread reflex, EMG responses and isometric force production. In conclusion, we demonstrate that reprogramming the muscle can be an effective strategy to improve reinnervation and functional outcomes after PNI.

| S-EPMC10802751 | biostudies-literature

Activation of skeletal muscle-resident glial cells upon nerve injury.

Project description:Here, we report on the identification of Itga7-expressing muscle-resident glial cells activated by loss of neuromuscular junction (NMJ) integrity. Gene expression analysis at the bulk and single-cell level revealed that these cells are distinct from Itga7-expressing muscle satellite cells. We show that a selective activation and expansion of Itga7+ glial cells occur in response to muscle nerve lesion. Upon activation, muscle glial-derived progenies expressed neurotrophic genes, including nerve growth factor receptor, which enables their isolation by FACS. We show that activated muscle glial cells also expressed genes potentially implicated in extracellular matrix remodeling at NMJs. We found that tenascin C, which was highly expressed by muscle glial cells, activated upon nerve injury and preferentially localized to NMJ. Interestingly, we observed that the activation of muscle glial cells by acute nerve injury was reversible upon NMJ repair. By contrast, in a mouse model of ALS, in which NMJ degeneration is progressive, muscle glial cells steadily increased over the course of the disease. However, they exhibited an impaired neurotrophic activity, suggesting that pathogenic activation of glial cells may be implicated in ALS progression.

| S-EPMC8119188 | biostudies-literature

Reactive Fibroblasts in Response to Optic Nerve Crush Injury.

Project description:Traumatic optic neuropathy leads to bidirectional degeneration of retinal ganglion cells and axons and results in optic nerve scaring, which inhibits the regeneration of damaged axons. Compared with its glial counterpart, the fibrotic response causing nerve scar tissue is poorly permissive to axonal regeneration. Using collagen1α1-GFP reporter mice, we characterize the development of fibrotic scar formation following optic nerve crush injury. We observe that perivascular collagen1α1 cells constitute a major cellular component of the fibrotic scar. We demonstrate that extracellular molecules and monocytes are key factors contributing to the pathogenesis of optic nerve fibrotic scar formation, with a previously unrecognized encapsulation of this scar. We also characterize the distribution of collagen1α1 cells in the retina after optic nerve crush injury based on in vivo and whole-mount retinal imaging. Our results identify collagen1α1 cells as a major component of fibrotic scarring following ONC and are a potential molecular target for promoting axonal regeneration after optic nerve injury.

| S-EPMC7933069 | biostudies-literature

Tanshinone IIA attenuates nerve structural and functional damage induced by nerve crush injury in rats.

Project description:After peripheral nerve crush injury, the fibers of distal nerve segments gradually disintegrate, and axons regrow from the proximal nerve segment, eventually reaching the target organ. However, the axon regeneration is generally not sufficient for the recovery of neurological function, so drug therapy is necessary. In the current study, we explored the effect of Tanshinone IIA in nerve regeneration in a sciatic nerve crush injury model using Sprague Dawley rats. The rats were administered 45 mg/kg of Tanshinone IIA once daily. Motor behavior and tibialis anterior muscle mass were assessed, and histological analysis of the sciatic nerve and lumbar spinal cord were conducted. The results showed that the administration of Tanshinone IIA improved nerve growth and motor function, and resulted in a marked decrease of neuronal death. The findings of this exploratory study suggest that Tanshinone IIA alleviates injury and boosts regeneration after nerve crush injury in a rat model of sciatic nerve injury.

| S-EPMC6107165 | biostudies-literature

Smooth Muscle Progenitor Cells Preserve the Erectile Function by Reducing Corporal Smooth Muscle Cell Apoptosis after Bilateral Cavernous Nerve Crush Injury in Rats.

Project description:Radical prostatectomy causes erectile dysfunction (ED) and irreversible morphologic changes, including induction of endothelial and smooth muscle cell (SMC) apoptosis in the corpus cavernosum (CC). The injection of smooth muscle progenitor cells (SPCs) thickens the vascular intima and has demonstrated therapeutic benefit in cardiovascular disease animal. Herein, we investigated the effect of SPCs on the recovery of erectile function (EF) in rat models with bilateral cavernous nerve (CN) injury. Twenty-four male Sprague-Dawley rats were randomized into sham, vehicle only, or SPC treatment groups. Rats in the SPC treatment and vehicle groups were subjected to bilateral CN injury before intracavernosal injection. Intracavernosal injections of SPCs increased all EF parameters at day 28 after injury and simultaneously reduced apoptosis of the SMCs. Ultrastructural analysis revealed that SPCs maintained the integrity of the CC by preserving the structure of the adherens junctions. Tracking transplanted SPCs labeled with EdU showed that transplanted SPCs remained in the CC 28 days after treatment. Intracavernosal SPC injection restored EF after bilateral CN injury by reducing SMC apoptosis, which favored the maintenance of the structure of adherens junctions and regulated the stability of corporal vessels. These findings demonstrate the therapeutic potential of SPCs for treating ED in humans.

| S-EPMC6885159 | biostudies-literature

re-innervation muscle in nerve crush rats

Project description:Two simulated nerve injury models in the rat tibial nerve were compared: the nerve was either cut (denervated, DN group) or crushed but with the nerve sheath intact (re-innervated, RN group). The control group had a preserved and intact tibial nerve. As the high expression of Myh3, Postn, Col6a1 and Cfi (nerve growth factors), the RN group demonstrated superior re-innervation as well. Both differentially expressed genes (DEGs) and proteins (DEPs) were enriched in the PPAR signaling pathway, as well as the energy metabolism.

2022-04-06 | PXD033031 |

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