Contralateral cytokine gene induction after peripheral nerve lesions: Dependence on the mode of injury and NMDA receptor signaling

Kleinschnitz, Christoph; Brinkhoff, Jörg; Sommer, Claudia; Stoll, Guido

doi:10.1016/j.molbrainres.2004.12.015

Cited by 66 publications

(53 citation statements)

References 28 publications

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“…IL-1β upregulates MMP-9 in optic nerve (Zhang and Chintala, 2004) and brain (Vecil et al, 2000), and NGF is known to induce MMP-9 in cultured neurons (Muir, 1994;Shubayev and Myers, 2004). The ability of the vehicle injection to cause the increase in MMP-9 is consistent with observations of mild inflammatory response to sham surgeries (Kleinschnitz et al, 2005).…”

Section: Discussionsupporting

confidence: 72%

Cytokine regulation of MMP-9 in peripheral glia: Implications for pathological processes and pain in injured nerve

Chattopadhyay

Myers

Janes

et al. 2007

Brain, Behavior, and Immunity

124

113

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Matrix metalloproteinase-9 (MMP-9) is an extracellular protease that is induced in Schwann cells hours after peripheral nerve injury and controls axonal degeneration and macrophage recruitment to the lesion. Here, we report a robust (90-fold) increase in MMP-9 mRNA within 24 h after rat sciatic nerve crush (1 to 60 days time-course). Using direct injection into a normal sciatic nerve, we identify the proinflammatory cytokines TNF-α and IL-1β as potent regulators of MMP-9 expression (Taqman qPCR, zymography). Myelinating Schwann cells produced MMP-9 in response to cytokine injection and crush nerve injury. MMP-9 gene deletion reduced unstimulated neuropathic nociceptive behavior after one week post-crush and preserved myelin thickness by protecting myelin basic protein (MBP) from degradation, tested by Western blot and immunofluorescence. These data suggest that MMP-9 expression in peripheral nerve is controlled by key proinflammatory cytokine pathways, and that its removal protects nerve fibers from demyelination and reduces neuropathic pain after injury.

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Section: Discussionsupporting

confidence: 72%

Cytokine regulation of MMP-9 in peripheral glia: Implications for pathological processes and pain in injured nerve

Chattopadhyay

Myers

Janes

et al. 2007

Brain, Behavior, and Immunity

124

113

View full text Add to dashboard Cite

show abstract

“…1). Although reports of contralateral side effects following nerve injury have been reported (Kleinschnitz et al, 2005;Koltzenburg et al, 1999), the data presented in Table 1 shows no difference in actual responses of the contralateral hind paw as assessed at days-2-16 post-CCI.…”

Section: Treatment With Clonidine Attenuates Cci-induced Thermal Hypementioning

confidence: 83%

Antinociception mediated by α2-adrenergic activation involves increasing tumor necrosis factor α (TNFα) expression and restoring TNFα and α2-adrenergic inhibition of norepinephrine release

et al. 2007

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The central component that establishes chronic pain from peripheral nerve injury is associated with increased tumor necrosis factor-α (TNFα) production in the brain. This study examined TNFα and its reciprocally permissive role with α 2 -adrenergic activation during peak and progressive decline of thermal hyperalgesia in sciatic nerve chronic constriction injury (CCI). Accumulation of TNFα mRNA (in situ hybridization) increases in the hippocampus and locus coeruleus during the onset of neuropathic pain and persists as hyperalgesia abates. Activation of α 2 -adrenergic receptors in control rats decreases TNFα mRNA accumulation in these brain regions. In contrast, during hyperalgesia, α 2 -adrenergic activation enhances TNFα mRNA accumulation. Whether this enhanced TNFα production is associated with changes in the regulation of norepinephrine (NE) release was tested. Hippocampal slices were electrically depolarized to evaluate α 2 -adrenergic and TNFα regulation of NE release. While inhibition of NE release by TNFα is maximal during peak hyperalgesia, it subsequently transforms to facilitate NE release. In addition, α 2 -adrenergic receptor activation with clonidine (0.2 mg/kg, i.p.) in CCI rats experiencing hyperalgesia restores TNFα and α 2 -adrenergic inhibition of NE release. While TNFα directs the development of hyperalgesia, it also directs its resolution. Transformed sensitivity to α 2 -adrenergic agonists during hyperalgesia demonstrates a mechanism for therapy.

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“…If we used the protocol like Piri et al by comparing the OH eye with the control eye, our conclusion would also indicate that OH caused down regulation of crystallins in the OH eye. There are increasing lines of evidence that unilateral nerve injury evokes contralateral responses [Bodeutsch et al, 1999;Kleinschnitz et al, 2005;Panagis et al, 2005]. Induction of OH in the right eyes may also cause stress in the contra-lateral left control eyes; and therefore, the use of the contralateral retina as a control in experimental glaucoma study is questionable.…”

Section: Discussionmentioning

confidence: 99%

Up‐regulation of crystallins is involved in the neuroprotective effect of wolfberry on survival of retinal ganglion cells in rat ocular hypertension model

Chiu

Zhou

Yeung

et al. 2010

J of Cellular Biochemistry

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Wolfberry (fruit of Lycium barbarum Linn) has been known for balancing 'Yin' and 'Yang' in the body, nourishing the liver and kidney, improving visual acuity for more than 2,500 years in oriental countries. The active components in wolfberry include L. barbarum polysaccharide (LBP), zeaxanthine, betaine, cerebroside and trace amounts of zinc, iron, and copper. Each of them confers distinct beneficial effects and together they help to explain widespread use of wolfberry in the eastern world. Earlier study reported the neuroprotective effects of LBP on retinal ganglion cell (RGC) in an experimental model of glaucoma and the underlying in vivo cellular mechanisms of LBP neuroprotection deserve further exploration. In this study, we adopted proteomics, functional genomics, to evaluate pharmacological effects of LBP on the neuronal survival pathways. Among the significantly changed proteins induced by LBP feeding on ocular hypertension (OH) retinas, only proteins in crystallin family were focused in this study. The proteomic results were further confirmed using the Western blotting of the retinas and immunohistochemical staining of the retinal sections. We demonstrated that neuroprotective effect of-wolfberry extract-LBP on the survival of RGCs may be mediated via direct up-regulation of neuronal survival signal betaB2-crystallin.

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Contralateral cytokine gene induction after peripheral nerve lesions: Dependence on the mode of injury and NMDA receptor signaling

Cited by 66 publications

References 28 publications

Cytokine regulation of MMP-9 in peripheral glia: Implications for pathological processes and pain in injured nerve

Cytokine regulation of MMP-9 in peripheral glia: Implications for pathological processes and pain in injured nerve

Antinociception mediated by α2-adrenergic activation involves increasing tumor necrosis factor α (TNFα) expression and restoring TNFα and α2-adrenergic inhibition of norepinephrine release

Up‐regulation of crystallins is involved in the neuroprotective effect of wolfberry on survival of retinal ganglion cells in rat ocular hypertension model

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