Increased Expression of Phospholipase D1 in the Sciatic Nerve of Rats With Experimental Autoimmune Neuritis

Shin, Taekyun; Min, D. S.; Ahn, Meejung; Son, Weon-Young; Matsumoto, Yoh

doi:10.1081/imm-120016238

Cited by 12 publications

(7 citation statements)

References 15 publications

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“…Furthermore, nitric oxide activates cyclooxygenase enzymes (Salvemini et al, 1993) and stimulated Schwann cells play a potential immunoregulatory role via the generation of NO, which suppresses T cell proliferation and ultimately induces T cell death (Gold et al, 1996). In line with these results, Schwann cells might be involved in PNS inflammation via the generation of COXs as well as NO and phospholipase D1 in response to inflammatory stimuli in sciatic nerves in autoimmune disease models (Kieseier et al, 2000;Shin et al, 2002).…”

Section: Discussionsupporting

confidence: 56%

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

Shin

Lee²,

Sim³

2003

Immunological Investigations

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The expression of both cyclooxygenase (COX)-1 and COX-2, which are representative enzymes in prostaglandin synthesis, was evaluated in the sciatic nerve of rats with experimental autoimmune neuritis (EAN). Western blot analysis showed that both COX-1 and COX-2 were significantly increased in the sciatic nerve at the peak stage of EAN and declined during the recovery stage. Vascular endothelial cells in normal sciatic nerves immunostained for both COX-1 and COX-2. COX-1 was mainly detected in macrophages, and not in other cell types, while COX-2 was detected in Schwann cells and axons as well as inflammatory macrophages in EAN lesions. This suggests that COXs are involved in the pathogenesis of peripheral demyelinating disease, including EAN, and the major cellular source of both COXs in EAN lesions is inflammatory macrophages. Furthermore, COX-2 is enhanced in some Schwann cells and neural elements, possibly mediating peripheral nervous system inflammation.

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Section: Discussionsupporting

confidence: 56%

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

Shin

Lee²,

Sim³

2003

Immunological Investigations

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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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“…Phospholipases (PLAs), a group of enzymes responsible for AA synthesis, have also emerged as possible mediators of the complex processes occurring during WD. PLAD1 immunoreactivity was found to be increased in SCs and macrophages in sciatic nerves in a rat model of experimental autoimmune neuritis [125] . Overexpression of PLA 2 could also be induced by experimental sciatic nerve injury.…”

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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Increased Expression of Phospholipase D1 in the Sciatic Nerve of Rats With Experimental Autoimmune Neuritis

Cited by 12 publications

References 15 publications

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

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

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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