Axon Outgrowth Enhanced by a Previous Nerve Injury

McQuarrie, Irvine G.; Grafstein, Bernice

doi:10.1001/archneur.1973.00490250071008

Cited by 249 publications

(133 citation statements)

References 9 publications

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…Preconditioning dramatically ramps up regenerative neurite outgrowth, a mechanism that involves, among others, heightened intracellular cAMP and increased expression of many regenerationassociated genes, including ␤III tubulin, GAP43/B50, and others (McQuarrie and Grafstein, 1973;McQuarrie et al, 1977;Forman et al, 1980;Oblinger and Lasek, 1984;Schreyer and Skene, 1991). Our prediction was that preconditioning would suppress PTEN activity, so that little added benefit would accrue from its inhibition.…”

Section: Inhibition Of Pten At the Protein Level In Vitro Increases Nmentioning

confidence: 91%

PTEN Inhibition to Facilitate Intrinsic Regenerative Outgrowth of Adult Peripheral Axons

Christie¹,

Webber²,

Martinez³

et al. 2010

Journal of Neuroscience

305

283

View full text Add to dashboard Cite

In vivo regeneration of peripheral neurons is constrained and rarely complete, and unfortunately patients with major nerve trunk transections experience only limited recovery. Intracellular inhibition of neuronal growth signals may be among these constraints. In this work, we investigated the role of PTEN (phosphatase and tensin homolog deleted on chromosome 10) during regeneration of peripheral neurons in adult Sprague Dawley rats. PTEN inhibits phosphoinositide 3-kinase (PI3-K)/Akt signaling, a common and central outgrowth and survival pathway downstream of neuronal growth factors. While PI3-K and Akt outgrowth signals were expressed and activated within adult peripheral neurons during regeneration, PTEN was similarly expressed and poised to inhibit their support. PTEN was expressed in neuron perikaryal cytoplasm, nuclei, regenerating axons, and Schwann cells. Adult sensory neurons in vitro responded to both graded pharmacological inhibition of PTEN and its mRNA knockdown using siRNA. Both approaches were associated with robust rises in the plasticity of neurite outgrowth that were independent of the mTOR (mammalian target of rapamycin) pathway. Importantly, this accelerated outgrowth was in addition to the increased outgrowth generated in neurons that had undergone a preconditioning lesion. Moreover, following severe nerve transection injuries, local pharmacological inhibition of PTEN or siRNA knockdown of PTEN at the injury site accelerated axon outgrowth in vivo. The findings indicated a remarkable impact on peripheral neuron plasticity through PTEN inhibition, even within a complex regenerative milieu. Overall, these findings identify a novel route to propagate intrinsic regeneration pathways within axons to benefit nerve repair.

show abstract

Section: Inhibition Of Pten At the Protein Level In Vitro Increases Nmentioning

confidence: 91%

PTEN Inhibition to Facilitate Intrinsic Regenerative Outgrowth of Adult Peripheral Axons

Christie¹,

Webber²,

Martinez³

et al. 2010

Journal of Neuroscience

305

283

View full text Add to dashboard Cite

show abstract

“…Studies of axonal regeneration in the sciatic nerve have shown that a conditioning lesion of the tibial nerve (a branch of the sciatic nerve) made 2 weeks before a sciatic nerve injury causes a significant increase in axon outgrowth. 40,41 Further work has shown that regeneration of dorsal root ganglion central processes into a peripheral nerve graft and regeneration of dorsal column fibers into a spinal cord lesion site is significantly improved by performing a peripheral nerve lesion. Thus, a preconditioning nerve lesion seems to increase the intrinsic regenerative ability of central axons by enhancing endogenous repair processes, such as elevation of intracellular cyclic adenosine monophosphate that allow axons to overcome myelin inhibition or by promoting of neuronal survival through attenuation of several injury-inducing mechanisms such as excitotoxicity, ion/pH imbalance, oxidative stress, metabolic dysfunction, and inflammation.…”

Section: -26mentioning

confidence: 99%

The Role of Diabetes Mellitus in the Clinical Presentation and Prognosis of Bell Palsy

Riga

Kefalidis

Danielides

2012

The Journal of the American Board of Family Medicine

View full text Add to dashboard Cite

Background: Bell palsy is considered to be an entrapment neuropathy resulting from inflammation, edema, and strangulation. Diabetes, hypertension, and hypercholesterolemia have all been related to microangiopathies. However, the relationship between the frequency, severity, and recovery course of Bell palsy in patients with these pathologies is a matter of controversy.Methods: Fifty-six patients with Bell palsy were evaluated according to the House-Brackmann grading system a few days after the onset of the disease and 6 months later and correlated to their hypertension, hypercholesterolemia, and diabetes records. Diabetes was evaluated by the use of serum glycosylated hemoglobin (HbA1c).Results: The 20 patients with abnormal HbA1c values were more frequently diagnosed with Bell palsy of grade V/VI (P ‫؍‬ .008; odds ratio, 4.7; 95% CI, 1.4 -15.2). However, their House-Brackmann scores were not found to be worse at the 6-month follow-up visit (P ‫؍‬ .9). No correlations were found for hypertension and hypercholesterolemia.Conclusions: A relationship between the severity of Bell palsy and abnormal HbA1c values seems to be demonstrated. However, the prognosis of these patients does not seem to be worse because at the 6-month follow-up visit they present similar scores to nondiabetic patients. (J Am Board Fam Med 2012;25:819 -826.)

show abstract

“…One of the best characterized examples of cytokine involvement in sympathetic neuroanatomical plasticity is their participation in neurite outgrowth following a conditioning lesion, such as axotomy (McQuarrie and Grafstein, 1973;McQuarrie et al, 1978). The conditioning lesion enhances the expression of cytokines of the gp130 family, which includes leukemia inhibitory factor, IL-6, IL-11, and oncostatin M, in tissues innervated by the axotomized sympathetic neurons and in the sympathetic neurons themselves (Hyatt Sachs et al, 2010).…”

Section: Comparison With the Conditioning Lesion Effectmentioning

confidence: 99%

Interleukin-17A Increases Neurite Outgrowth from Adult Postganglionic Sympathetic Neurons

Chisholm

Cervi²,

Nagpal³

et al. 2012

J. Neurosci.

View full text Add to dashboard Cite

Axon Outgrowth Enhanced by a Previous Nerve Injury

Abstract: In the sciatic nerve of adult mice, the rate of axonal elongation following nerve excision was 27% faster than normal if the nerve had been crushed two weeks before the excision.(29: [53][54][55] 1973)

Cited by 249 publications

References 9 publications

PTEN Inhibition to Facilitate Intrinsic Regenerative Outgrowth of Adult Peripheral Axons

PTEN Inhibition to Facilitate Intrinsic Regenerative Outgrowth of Adult Peripheral Axons

The Role of Diabetes Mellitus in the Clinical Presentation and Prognosis of Bell Palsy

Interleukin-17A Increases Neurite Outgrowth from Adult Postganglionic Sympathetic Neurons

Contact Info

Product

Resources

About