Neuropathic Pain and Nerve Growth Factor in Chemotherapy-Induced Peripheral Neuropathy: Prospective Clinical-Pathological Study

Velasco, Roser; Navarro, Xavier; Gil-Gil, Miguel; Herrando-Grabulosa, Mireia; Calls, Aina; Bruna, Jordi

doi:10.1016/j.jpainsymman.2017.04.021

Cited by 45 publications

(38 citation statements)

References 36 publications

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“…The occurrence and development of DNP involves a variety of biochemical factors and alterations in anatomic structures in the peripheral nervous system and central nervous system [14]. Continuous hyperglycemia as the key initiating factor, could eventually provoke heightened excitability of peripheral nerve sensory and spinal dorsal horn neurons by controlling neuronal voltage-gated ion channels and affecting the production of nerve growth factor (NGF), leading to the spontaneous discharge of neurons and increased central sensitization, which is the basis of neuropathic pain [15, 16]. In addition, abundant studies provide strong evidence that the inflammatory microenvironment and the release of inflammatory mediators such as TNF-α are the precipitating factors for DNP development [17].…”

Section: Discussionmentioning

confidence: 99%

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

Jiang

Wang

et al. 2019

J Inflamm

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Background Emerging evidence has demonstrated that inflammation is involved in the occurrence and development of diabetic neuropathic pain (DNP). The anti-inflammatory property of interleukin (IL)-35 makes it a promising candidate to block the pain perception. The present study was undertaken to investigate whether IL-35 could attenuate DNP in streptozotocin (STZ)-induced rat model and its potential mechanism. Methods The rat model of DNP was established by a single STZ injection followed by measurements of fasting blood glucose and insulin. Fourteen days after STZ injection, DNP rats were intrathecally injected with IL-35, c-Jun N-terminal kinase (JNK) inhibitor or activator or dimethylsulfoxide (DMSO) as vehicle control, respectively. The mechanical allodynia was assayed to evaluate the therapeutic effect of IL-35. In mechanism study, the serum and protein levels of inflammatory cytokines using ELISA and western blotting and the activation of JNK signaling were further evaluated by quantitative reverse transcription PCR (qRT-PCR). Histopathologic changes were evaluated by Nissl staining. Apoptosis was examined using TUNEL staining. Results DNP rats exhibited increased fasting blood glucose and insulin levels and reduced insulin sensitivity index (ISI). Intrathecal injection of IL-35 reduced accumulation of pro-inflammatory cytokines in the spinal cord of DNP rats. Furthermore, IL-35 displayed anti-inflammatory and anti-apoptotic effects via inhibition of JNK pathway. Conclusion IL-35 treatment mitigated DNP via downregulating JNK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

Jiang

Wang

et al. 2019

J Inflamm

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“…Therefore, given the properties of the [Ca2+] i fluctuations we have identified, they would make a good candidate for the neural substrate of shooting pain. In a cohort of chemotherapy-induced peripheral neuropathy (CIPN) patients, some of whom reported shooting or burning pain in the hands or feet, serum nerve growth factor (NGF) levels were much higher compared with patients with painless or absent CIPN (36). Therefore, there is a precedent for the correlation of neurotrophic factors related to BDNF to the incidence of shooting pain.…”

Section: Discussionmentioning

confidence: 99%

Chronic BDNF simultaneously inhibits and unmasks superficial dorsal horn neuronal activity

Alles

Odem

et al. 2020

Preprint

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Brain-derived neurotrophic factor (BDNF) is critically involved in the pathophysiology of chronic pain. However, the mechanisms of BDNF action on specific neuronal populations in the spinal superficial dorsal horn (SDH) requires further study. We used chronic BDNF treatment (200 ng/ml, 5-6 days) of defined-medium, serum-free spinal organotypic cultures to study intracellular calcium ([Ca2+]i) fluctuations. A detailed quantitative analysis of these fluctuations using the Frequency-independent biological signal identification (FIBSI) program revealed that BDNF simultaneously depressed activity in some SDH neurons while it unmasked a particular subpopulation of 'silent' neurons causing them to become spontaneously active. Blockade of gap junctions disinhibited a subpopulation of SDH neurons and reduced BDNF-induced synchrony in BDNF-treated cultures. BDNF reduced neuronal excitability by measuring spontaneous excitatory postsynaptic currents. This was similar to the depressive effect of BDNF on the [Ca2+]i fluctuations. This study reveals novel regulatory mechanisms of SDH neuronal excitability in response to BDNF.

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“…Some clinical treatments provide ideal models with which to evaluate changes in fiber density and reinnervation. Examples include: (1) Nerve damage treatments, including post-LASIK—a procedure that severs corneal nerves [130,131]; (2) toxic treatments, such as chemotherapy [41], in which CCM has the potential to be more sensitive than IESB [10]; and (3) endocrine-related treatments in diabetic neuropathy. For direct trauma/surgery to the skin, IESB has not been used in humans but has been observed in entrapment neuropathy in rats, a model for chronic compression injury [132].…”

Section: Skin Biopsy Vs Corneal Microscopymentioning

confidence: 99%

“…In chronic pain conditions, nerve morphology alterations in the skin and cornea have been correlated with disease condition in both the peripheral and central nervous system [6,7,8]. However, these skin biopsy findings are not universal for all neuropathic pain conditions [9,10]. While skin biopsies have been sensitive for many small fiber or mixed neuropathies, the sensitivity and specificity of corneal nerve evaluation using corneal confocal microscopy (CCM) is less well defined.…”

Section: Introductionmentioning

confidence: 99%

C-Fiber Assays in the Cornea vs. Skin

Moulton

Borsook

2019

Brain Sciences

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C-fibers are unmyelinated nerve fibers that transmit high threshold mechanical, thermal, and chemical signals that are associated with pain sensations. This review examines current literature on measuring altered peripheral nerve morphology and discusses the most relevant aspects of corneal microscopy, especially whether corneal imaging presents significant method advantages over skin biopsy. Given its relative merits, corneal confocal microscopy would seem to be a more practical and patient-centric approach than utilizing skin biopsies.

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Neuropathic Pain and Nerve Growth Factor in Chemotherapy-Induced Peripheral Neuropathy: Prospective Clinical-Pathological Study

Cited by 45 publications

References 36 publications

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

Chronic BDNF simultaneously inhibits and unmasks superficial dorsal horn neuronal activity

C-Fiber Assays in the Cornea vs. Skin

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