Key Glycolytic Metabolites in Paralyzed Skeletal Muscle Are Altered Seven Days after Spinal Cord Injury in Mice

Graham, Zachary A.; Siedlik, Jacob A.; Harlow, Lauren; Sahbani, Karim; Bauman, William A.; Tawfeek, Hesham A.; Cardozo, Christopher P.

doi:10.1089/neu.2018.6144

Cited by 16 publications

(20 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Muscle atrophy occurs rapidly in female mice after a complete SCI as 20–25% of gastrocnemius mass is lost by 7 d with additional losses seen at 28 d post‐SCI (Graham et al, 2019). A complete transection rarely occurs in humans, however, and incomplete SCI is likely to be associated with varying amounts of atrophy depending on injury severity and recovery and rehabilitation.…”

Section: Discussionmentioning

confidence: 99%

A 50 kdyne contusion spinal cord injury with or without the drug SS‐31 was not associated with major changes in muscle mass or gene expression 14 d after injury in young male mice

et al. 2021

Self Cite

View full text Add to dashboard Cite

Spinal cord injury (SCI) leads to rapid muscle atrophy due to paralysis/paresis and subsequent disuse. SS‐31 is a mitochondrial‐targeting peptide that has shown efficacy in protecting skeletal muscle mass and function in non‐SCI models of muscle wasting. We aimed to determine if SS‐31 could prevent muscle loss after SCI. Male C57BL/6 mice aged 9 weeks underwent sham surgery or 50 kdyne contusion SCI and were administered daily injections of vehicle or 5 mg/kg SS‐31 for 14 d. Both SCI groups had sustained losses in body mass compared to Sham animals and ~10% reductions in gastrocnemius, plantaris and tibialis anterior muscle mass after SCI with no clear effect of SS‐31. Measurements of protein synthesis in the soleus and plantaris were similar among all groups. mRNA expression of atrophy‐associated proinflammatory cytokines was also similar among all groups. There was elevation in MYH7 mRNA and a statistical reduction in MYH2 mRNA expression in the SCI+SS‐31 animals compared to Sham animals. There was an SCI‐induced reduction in mRNA expression of the E3 ligase FBXO32 (MAFbx), but no effect of SS‐31. In summary, a 50 kdyne contusion SCI was able to reduce body mass but was not associated with substantial muscle atrophy or alterations in gene expression profiles associated with muscle health and function 14 d post‐injury. SS‐31 was not associated with protection against SCI‐related changes in body or muscle mass, protein synthesis or gene expression in hindlimb muscles.

show abstract

Section: Discussionmentioning

confidence: 99%

A 50 kdyne contusion spinal cord injury with or without the drug SS‐31 was not associated with major changes in muscle mass or gene expression 14 d after injury in young male mice

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…A 2008 study in 42 SCI patients found that incidence of insulin resistance did not depend on injury severity or location, with equal levels amongst para-and tetraplegics and those with complete and incomplete injuries (Huang et al, 2008). Changes in muscle use and innervation have been suggested to be a primary influence on the development of insulin resistance (Graham et al, 2019), although aberrant activation of the sympathetic nervous system may also play a role (Karlsson, 1999). Increasing exercise can alleviate this condition, reducing blood glucose and increasing insulin sensitivity (Jeon et al, 2002;Koury et al, 2013).…”

Section: No Hypoglycemiamentioning

confidence: 99%

Role of Insulin in Neurotrauma and Neurodegeneration: A Review

et al. 2020

View full text Add to dashboard Cite

Insulin is a hormone typically associated with pancreatic release and blood sugar regulation. The brain was long thought to be "insulin-independent," but research has shown that insulin receptors (IR) are expressed on neurons, microglia and astrocytes, among other cells. The effects of insulin on cells within the central nervous system are varied, and can include both metabolic and non-metabolic functions. Emerging data suggests that insulin can improve neuronal survival or recovery after trauma or during neurodegenerative diseases. Further, data suggests a strong antiinflammatory component of insulin, which may also play a role in both neurotrauma and neurodegeneration. As a result, administration of exogenous insulin, either via systemic or intranasal routes, is an increasing area of focus in research in neurotrauma and neurodegenerative disorders. This review will explore the literature to date on the role of insulin in neurotrauma and neurodegeneration, with a focus on traumatic brain injury (TBI), spinal cord injury (SCI), Alzheimer's disease (AD) and Parkinson's disease (PD).

show abstract

“…It is possible that treatments for SCI altering systemic metabolic activity (e.g. calorific restriction or reductions in glycolytic function) (Jeong et al 2011;Graham et al 2019) have been successful in part because of the effect that they have had on peripheral muscle. This indicates that combining treatments that (i) aid functional plasticity and connectivity at the spinal level; (ii) maintain capillarity though passive stretch; and (iii) increase oxidative phosphorylation in paralysed muscles (e.g.…”

Section: Discussionmentioning

confidence: 99%

Oxygen transport kinetics underpin rapid and robust diaphragm recovery following chronic spinal cord injury

Warren

Kissane

Egginton

et al. 2020

The Journal of Physiology

View full text Add to dashboard Cite

Spinal treatment can restore diaphragm function in all animals 1 month following C2 hemisection induced paralysis. Greater recovery occurs the longer after injury the treatment is applied. r Through advanced assessment of muscle mechanics, innovative histology and oxygen tension modelling, we have comprehensively characterized in vivo diaphragm function and phenotype. r Muscle work loops reveal a significant deficit in diaphragm functional properties following chronic injury and paralysis, which are normalized following restored muscle activity caused by plasticity-induced spinal reconnection. r Injury causes global and local alterations in diaphragm muscle vascular supply, limiting oxygen diffusion and disturbing function. Restoration of muscle activity reverses these alterations, restoring oxygen supply to the tissue and enabling recovery of muscle functional properties. r There remain metabolic deficits following restoration of diaphragm activity, probably explaining only partial functional recovery. We hypothesize that these deficits need to be resolved to restore complete respiratory motor function.

show abstract

Key Glycolytic Metabolites in Paralyzed Skeletal Muscle Are Altered Seven Days after Spinal Cord Injury in Mice

Cited by 16 publications

References 56 publications

A 50 kdyne contusion spinal cord injury with or without the drug SS‐31 was not associated with major changes in muscle mass or gene expression 14 d after injury in young male mice

A 50 kdyne contusion spinal cord injury with or without the drug SS‐31 was not associated with major changes in muscle mass or gene expression 14 d after injury in young male mice

Role of Insulin in Neurotrauma and Neurodegeneration: A Review

Oxygen transport kinetics underpin rapid and robust diaphragm recovery following chronic spinal cord injury

Contact Info

Product

Resources

About