scholarly journals Role of the Excitability Brake Potassium Current I KD in Cold Allodynia Induced by Chronic Peripheral Nerve Injury

2017 ◽  
Vol 37 (12) ◽  
pp. 3109-3126 ◽  
Author(s):  
Alejandro González ◽  
Gonzalo Ugarte ◽  
Carlos Restrepo ◽  
Gaspar Herrera ◽  
Ricardo Piña ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Potassium Current ◽  
Cold Allodynia

Role of Histamine H3 and H4 Receptors in Mechanical Hyperalgesia following Peripheral Nerve Injury

2007 ◽  
Vol 14 (6) ◽  
pp. 317-325 ◽  
Author(s):  
Fiona M. Smith ◽  
Hila Haskelberg ◽  
David J. Tracey ◽  
Gila Moalem-Taylor
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Mechanical Hyperalgesia

scholarly journals Role of IL-10 in Resolution of Inflammation and Functional Recovery after Peripheral Nerve Injury

2015 ◽  
Vol 35 (50) ◽  
pp. 16431-16442 ◽  
Author(s):  
B. Siqueira Mietto ◽  
A. Kroner ◽  
E. I. Girolami ◽  
E. Santos-Nogueira ◽  
J. Zhang ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Functional Recovery ◽  
Peripheral Nerve Injury ◽  
Resolution Of Inflammation

Increase of interleukin-6 mRNA in the spinal cord following peripheral nerve injury in the rat: potential role of IL-6 in neuropathic pain

1998 ◽  
Vol 62 (2) ◽  
pp. 228-235 ◽  
Author(s):  
Janice L Arruda ◽  
Raymond W Colburn ◽  
Amy J Rickman ◽  
Maria D Rutkowski ◽  
Joyce A DeLeo
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Interleukin 6 ◽  
Peripheral Nerve Injury ◽  
Potential Role

scholarly journals SIRT6 inhibition delays peripheral nerve recovery by suppressing migration, phagocytosis and M2-polarization of macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ying Zou ◽  
Jiaqi Zhang ◽  
Jiawei Xu ◽  
Lanya Fu ◽  
Yizhou Xu ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Macrophage Polarization ◽  
Nerve Degeneration ◽  
M2 Polarization ◽  
M1 Macrophage ◽  
Nerve Recovery

Abstract Background Silent information regulator 6 (SIRT6) is a mammalian homolog of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin family. Prior evidences suggested that the anti-inflammatory function of SIRT6 after spinal cord and brain injury, and it plays a crucial role in macrophages polarization of adipose tissue and skin. However, the role of SIRT6 in macrophages involved peripheral nerve injury is still unknown. Given the prominent role of macrophages in peripheral nerve recovery, we aim to investigate the role of SIRT6 in the regulation of phenotypes shift and functions in macrophages after peripheral nerve injury. Results In the present study, we first identified a significant increase of SIRT6 expression during nerve degeneration and macrophages phagocytosis. Next, we found nerve recovery was delayed after SIRT6 silencing by injected shRNA lentivirus into the crushed sciatic nerve, which exhibited a reduced expression of myelin-related proteins (e.g., MAG and MBP), severer myoatrophy of target muscles, and inferior nerve conduction compared to the shRNA control injected mice. In vitro, we found that SIRT6 inhibition by being treated with a selective inhibitor OSS_128167 or lentivirus transfection impairs migration and phagocytosis capacity of bone marrow-derived macrophages (BMDM). In addition, SIRT6 expression was discovered to be reduced after M1 polarization, but SIRT6 was enhanced after M2 polarization in the monocyte-macrophage cell line RAW264.7 and BMDM. Moreover, SIRT6 inhibition increased M1 macrophage polarization with a concomitant decrease in M2 polarization both in RAW264.7 and BMDM via activating NF-κB and TNF-α expression, and SIRT6 activation by UBCS039 treatment could shift the macrophages from M1 to M2 phenotype. Conclusion Our findings indicate that SIRT6 inhibition impairs peripheral nerve repair through suppressing the migration, phagocytosis, and M2 polarization of macrophages. Therefore, SIRT6 may become a favorable therapeutic target for peripheral nerve injury.

scholarly journals Role of Myc Proto-Oncogene as a Transcriptional Hub to Regulate the Expression of Regeneration-Associated Genes following Preconditioning Peripheral Nerve Injury

2020 ◽  
Vol 41 (3) ◽  
pp. 446-460
Author(s):  
Hae Young Shin ◽  
Min Jung Kwon ◽  
Eun Mi Lee ◽  
Kyung Kim ◽  
Young Joo Oh ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury

scholarly journals ARA290, a Peptide Derived from the Tertiary Structure of Erythropoietin, Produces Long-term Relief of Neuropathic Pain

2011 ◽  
Vol 115 (5) ◽  
pp. 1084-1092 ◽  
Author(s):  
Maarten Swartjes ◽  
Aurora Morariu ◽  
Marieke Niesters ◽  
Michael Brines ◽  
Anthony Cerami ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Tertiary Structure ◽  
Cold Allodynia ◽  
Cardiovascular Side Effects ◽  
Common Receptor ◽  
Rats And Mice

Background Exogenous erythropoietin inhibits development of allodynia in experimental painful neuropathy because of its antiinflammatory and neuroprotective properties at spinal, supraspinal, and possibly peripheral sites. The authors assess the effect of a nonhematopoietic erythropoietin analog, ARA290, on tactile and cold allodynia in a model of neuropathic pain (spared nerve injury) in rats and mice lacking the β-common receptor (βcR mice), a component of the receptor complex mediating tissue protection. Methods Twenty-four hours after peripheral nerve injury, rats and mice were injected with ARA290 or vehicle (five 30-μg/kg intraperitoneal injections at 2-day intervals, followed by once/week, n = 8/group). In a separate group of eight rats, ARA290 treatment was restricted to five doses during the initial 2 weeks after surgery. Results In rats, irrespective of treatment paradigm, ARA290 produced effective, long-term (as long as 15 weeks) relief of tactile and cold allodynia (P < 0.001 vs. vehicle-treated animals). ARA290 was effective in wild-type mice, producing significant relief of allodynia. In contrast, in βcR mice no effect of ARA290 was observed. Conclusions ARA290 produces long-term relief of allodynia because of activation of the β-common receptor. It is argued that relief of neuropathic pain attributable to ARA290 treatment is related to its antiinflammatory properties, possibly within the central nervous system. Because ARA290, in contrast to erythropoietin, is devoid of hematopoietic and cardiovascular side effects, ARA290 is a promising new drug in the prevention of peripheral nerve injury-induced neuropathic pain in humans.

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