Involvement of Cyclooxygenase‐1 and ‐2 in the Sciatic Nerve of Rats with Experimental Autoimmune Neuritis

Shin, Taekyun; Lee, Yongduk; Sim, Ki‐Bum

doi:10.1081/imm-120022973

Cited by 10 publications

(8 citation statements)

References 14 publications

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“…Such negative findings suggest that COX-1 expression in trigeminal primary afferent nociceptive neurons, if present, may be limited to the cell body and not transported to the nociceptor’s peripheral endings in the dura. Our findings are supported by other studies which also failed to detect COX-1 expression in peripheral nerves [10, 12, 19], but are in contrast to a recent study showing COX-1 immunoreactivity in large cutaneous nerve branches, as well as small intradermal nerve bundles and nerve endings [13]. Such discrepancies may be due to differences between the innervation of the skin and the dura or more generally between trigeminal and non-trigeminal sensory innervations.…”

Section: Discussionsupporting

confidence: 85%

Localization of COX-1 and COX-2 in the intracranial dura mater of the rat

Zhang

Kainz

Jakubowski

et al. 2009

Neuroscience Letters

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Primary headaches such as migraine can be aborted by systemic administration of non-steroidal antiinflammatory drugs (NSAIDs), potentially through the non-selective inhibition of cyclooxygenase (COX) activity in the intracranial meninges. In this study we have used single and double labeling immunohistochemistry to examine the distribution of the COX-1 and COX-2 isoforms in the intracranial dura mater of the rat and identify cell types that express them. COX-1 immunoreactivity was found in medium and small dural blood vessels and was co-expressed with the endothelial cell markers vimentin and the endothelial isoform of nitric oxide synthase (ecNOS). COX-1 was also found to be present in most dural mast cells. COX-2 was mainly expressed in ED2-positive resident dural macrophages. Constitutive COX-2 expression was also found in some axonal profiles, many of which were co-labeled with the nociceptor peptide marker CGRP. The findings suggest that NSAIDs may abort headache, at least in part, by inhibiting either neuronal or non-neuronal COX activity in the dura mater.

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Section: Discussionsupporting

confidence: 85%

Localization of COX-1 and COX-2 in the intracranial dura mater of the rat

Zhang

Kainz

Jakubowski

et al. 2009

Neuroscience Letters

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“…Active EAN was induced in the rats as described earlier ( Shin et al, 2002; 2003 ; Ahn et al, 2004a; 2004b ; Moon et al, 2005 ) . Briefly, each rat was injected in both hind footpads with an emulsion containing 100 µg SP26, a neuritogenic peptide homologous to amino acids 53–78 of bovine myelin P2 protein (Shimadzu, Kyoto, Japan), and complete Freund's adjuvant (CFA; Mycobacterium tuberculosis H37Ra, 5 mg/ml).…”

Section: Methodsmentioning

confidence: 99%

Glial cell line‐derived neurotrophic factor is expressed by inflammatory cells in the sciatic nerves of Lewis rats with experimental autoimmune neuritis

Ahn

Jin

Moon

et al. 2010

J Peripheral Nervous Sys

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Neurotrophic factors, including glial cell line-derived neurotrophic factor (GDNF), have been known to play a role in neuroprotection in the injured peripheral nervous system (PNS). To evaluate the involvement of GDNF in experimental autoimmune neuritis (EAN) pathogenesis, the expression of GDNF in rat sciatic nerves with EAN was studied. Western blot analysis showed that the level of GDNF protein significantly increased 1.8-fold at the paralytic stage of EAN at day 12 post-immunization (PI) (p < 0.01), and its level further increased approximately 2.5-fold at day 21 PI (p < 0.001) in the sciatic nerves of EAN-affected rats compared with those of control rats, and then declined thereafter at day 28 PI. Immunohistochemical analysis showed that axons and Schwann cells constitutively contained GDNF in normal controls. In sciatic nerves with EAN at day 12 PI, GDNF was immunostained in infiltrating inflammatory cells including macrophages and T cells. Collectively, we postulate that GDNF plays a regulatory role in EAN paralysis. A paradoxical role of inflammatory cells to ameliorate PNS inflammation remains to be further studied in EAN, an animal model of human demyelinating disease.

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“…However, the fact that local COX-2-mediated PG production is dramatically increased after nerve injury, and that PGs are capable of modulating the expression of pro-and anti-inflammatory cytokines, suggests that there might be an important role for COX-2 and PGs in the evolution of nerve degeneration and regeneration [116] . Both COX-1 and COX-2 expression is increased in macrophages and SCs in animal models of inflammatory demyelinating diseases [117] . A role for COX-1 expression in microglia and macrophages in tissue remodeling dur-ing WD in the spinal cord has also been proposed [118] .…”

Section: Aa and Its Metabolitesmentioning

confidence: 99%

Molecular Inflammatory Mediators in Peripheral Nerve Degeneration and Regeneration

Cámara-Lemarroy

Garza²,

Fernández-Garza³

2010

Neuroimmunomodulation

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Wallerian degeneration, the self-destructive set of cellular and molecular processes by which degenerating axons and myelin are cleared after injury, is initiated by macrophages and Schwann cells. Molecular inflammatory mediators such as cytokines (IL-1, IL-6, IL-10, and TNF-α, among others), transcription factors (NF-ĸB, c-Jun), the complement system and arachidonic acid metabolites have been shown to modulate these processes in various studies. However, the exact role that each of these mediators plays during axonal degeneration and regeneration has not been fully established. Understanding the molecular basis of these interactions between the immune system and peripheral nerve injury would open the possibility of targeting these inflammatory mediators as therapeutic interventions. In this review we attempt to integrate the current evidence generated around this issue, and to explore the therapeutic possibilities that arise.

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Involvement of Cyclooxygenase‐1 and ‐2 in the Sciatic Nerve of Rats with Experimental Autoimmune Neuritis

Cited by 10 publications

References 14 publications

Localization of COX-1 and COX-2 in the intracranial dura mater of the rat

Localization of COX-1 and COX-2 in the intracranial dura mater of the rat

Glial cell line‐derived neurotrophic factor is expressed by inflammatory cells in the sciatic nerves of Lewis rats with experimental autoimmune neuritis

Molecular Inflammatory Mediators in Peripheral Nerve Degeneration and Regeneration

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