Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1160713 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30659440_1.fastq.gz | Fastqsanger.gz | |||
| SRR30659440_2.fastq.gz | Fastqsanger.gz | |||
| SRR30659441_1.fastq.gz | Fastqsanger.gz | |||
| SRR30659441_2.fastq.gz | Fastqsanger.gz | |||
| SRR30659442_1.fastq.gz | Fastqsanger.gz |
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Project description:The pathophysiology of recurrent laryngeal nerve (RLN) transection injury is rare in that it is characteristically followed by a high degree of spontaneous reinnervation, with reinnervation of the laryngeal adductor complex (AC) preceding that of the abducting posterior cricoarytenoid (PCA) muscle. Here, we aim to elucidate the differentially expressed myogenic factors following RLN injury that may be at least partially responsible for the spontaneous reinnervation. F344 male rats underwent RLN injury or sham surgery (n=12). One week after RLN injury, larynges were harvested following euthanasia. mRNA was extracted from PCA and AC muscles bilaterally, and microarray analysis was performed using a full rat genome array. Microarray analysis of denervated AC and PCA muscles demonstrated dramatic differences in gene expression profiles, with 205 individual probes that were differentially expressed between the denervated AC and PCA muscles, and only 14 genes with similar expression patterns. The differential expression patterns of the AC and PCA suggest different mechanisms of reinnervation. The PCA showed the gene patterns of Wallerian degeneration, while the AC expressed the gene patterns of reinnervation by adjacent axonal sprouting. This finding may reveal important therapeutic targets applicable to RLN and other peripheral nerve injuries. Compare mRNA expression from injured tissue (recurrent laryngeal nerve transection injury) to normal tissue from two tissues laryngeal adductor complex and posterior cricoarytenoid muscles.
2016-07-01 | E-GEOD-72361 | biostudies-arrayexpress
Project description:The pathophysiology of recurrent laryngeal nerve (RLN) transection injury is rare in that it is characteristically followed by a high degree of spontaneous reinnervation, with reinnervation of the laryngeal adductor complex (AC) preceding that of the abducting posterior cricoarytenoid (PCA) muscle. Here, we aim to elucidate the differentially expressed myogenic factors following RLN injury that may be at least partially responsible for the spontaneous reinnervation. F344 male rats underwent RLN injury or sham surgery (n=12). One week after RLN injury, larynges were harvested following euthanasia. mRNA was extracted from PCA and AC muscles bilaterally, and microarray analysis was performed using a full rat genome array. Microarray analysis of denervated AC and PCA muscles demonstrated dramatic differences in gene expression profiles, with 205 individual probes that were differentially expressed between the denervated AC and PCA muscles, and only 14 genes with similar expression patterns. The differential expression patterns of the AC and PCA suggest different mechanisms of reinnervation. The PCA showed the gene patterns of Wallerian degeneration, while the AC expressed the gene patterns of reinnervation by adjacent axonal sprouting. This finding may reveal important therapeutic targets applicable to RLN and other peripheral nerve injuries.
2016-07-01 | GSE72361 | GEO
Project description:Peripheral nerve repair and functional recovery depend on the rate of nerve regeneration and the quality of target reinnervation. It is important to fully understand the cellular and molecular basis underlying the specificity of peripheral nerve regeneration, which means the achieving of respective correct pathfinding and accurate target reinnervation for regrowing motor and sensory axons. In this study, a quantitative proteomic technique, based on isobaric tags for relative and absolute quantitation (iTRAQ) was used to profile the protein expression pattern between single motor and sensory nerves at 14 days after peripheral nerve transection. Among a total of 1259 proteins identified, 176 proteins showed the differential expressions between injured motor and sensory nerves. Quantitative real-time RT-PCR and Western blot analysis were applied to validate the proteomic data on representative differentially expressed proteins. Functional categorization indicated that differentially expressed proteins were linked to a diverse array of molecular functions, including axonogenesis, response to axon injury, tissue remodeling, axon ensheathment, cell proliferation and adhesion, vesicle-mediated transport, response to oxidative stress, internal signal cascade, and macromolecular complex assembly, which might play an essential role in peripheral motor and sensory nerve regeneration. Overall, we hope that the proteomic database obtained in this study could serve as a solid foundation for the comprehensive investigation of differentially expressed proteins between injured motor and sensory nerves and for the mechanism elucidation of the specificity of peripheral nerve regeneration.
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Project description:Peripheral nerve injuries lead to diminished function and pain via nociplastic phenomena. We propose a new strategy called Directed Functional Reinnervation, in which nerves are reassigned to new peripheral targets with the goal of altering circuit function. Here, we redirect pure sensory nerves into skeletal muscle grafts to curb nociplasticity and provide benign or useful inputs for prosthetic applications. Electrophysiological characterization of the functional signaling capabilities demonstrated robust afferent responses to mechanical stimuli. Immunofluorescence staining of the saphenous nerve graft indicated widespread innervation of various synapses within the muscle. With immediate graft placement, the injured nerves’ dorsal root ganglia revealed comparable levels of nociceptive markers to uninjured nerves, suggesting a molecular basis for the prevention of pain sensitization. These findings support the use of skeletal muscle grafts for the alleviation of neuropathic pain and use as a sensory transmitter in conjunction with neural interfaces.
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Project description:Aging is associated with delayed skeletal muscle repair and regeneration. Loss of innervation occurs after degenerative muscle injury, however, the extent of denervation, whether the kinetics of reinnervation changes with aging, and the cellular consequences of neuromuscular junction (NMJ) disruption in adult and aged muscle have not been explored. Here we show after degenerative muscle injury progressive denervation and delayed reinnervation in aged compared to adult muscle. Using confocal microscopy and 3-D image rendering we found a relationship between innervation and myofiber size in aged regenerating muscle. Although timely inhibition of pro-inflammatory Ccr2 activity after degenerative muscle injury improved aged regenerated myofiber size, this was not associated with an increase in reinnervation. In contrast, single cell RNA sequencing (scRNASeq) analysis revealed denervation triggers an inflammatory response in target muscles regardless of age; however, pro-inflammatory signaling predominated in aged macrophages and fibroadipogenic progenitors (FAPs) compared to a pro-regenerative response in adult cells. Thus, denervation and delayed reinnervation of NMJs after injury is a feature of persistent pro-inflammatory signals associated with delayed repair and regeneration of aged muscle.
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