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

Chattopadhyay, Sharmila; Myers, Robert R.; Janes, Julie R.; Shubayev, Veronica I.

doi:10.1016/j.bbi.2006.10.015

Cited by 122 publications

(121 citation statements)

References 62 publications

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“…Once released, these neuropeptides bind to their receptors on neurons and glia and trigger downstream signaling events leading to central sensitization [12][13][14][15][16][17][18][19][20][21][22]. Neuronal activity increases endovanilloid levels during chronic pain conditions, which are synthesized and released on demand [42][43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

“…It is likely that peripheral injury-induced neuronal activity releases Calcitonin GeneRelated Peptide (CGRP) and Substance P (SP) from presynaptic nerve terminals and activation of glia influencing the synthesis and release of anandamide and proand anti-inflammatory mediators. Anandamide and inflammatory mediators act retrogradely to modulate synaptic transmission and TRPV1 expression and function, respectively [12][13][14][15][16][17][18][19][20][21][22]. Resiniferatoxin (RTX) is an ultrapotent TRPV1 agonist, which activates TRPV1 in an irreversible manner.…”

Section: Transient Receptor Potential Vanilloid 1 (Trpv1) Is a Camentioning

confidence: 99%

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Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Yu¹,

Premkumar²

2015

TOPAINJ

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Transient Receptor Potential Vanilloid 1 (TRPV1) expressed in peripheral terminals is responsible for transducing thermal and chemical nociception. Role of TRPV1 expressed in the central terminals is not clear, however, its activation modulates synaptic transmission and contributes to central sensitization. In this study, we have determined the role of TRPV1 expressed in the peripheral and central terminals using resiniferatoxin (RTX), a potent TRPV1 agonist. A single intraplantar injection of RTX, within two days induced loss of capsaicin-induced nocifensive behavior and enhanced response latency to hot plate, which recovered over a period of two months. RTX treatment resulted in the ablation of peripheral TRPV1 expressing fibers in paw skin, which regenerated over the same time period. On the other hand, a single dose of intrathecal administration of RTX, within two days caused thermal hypoalgesia. RTX treatment ablated TRPV1 expressing central sensory nerve terminals. Intriguingly, in contrast to peripheral nerve terminal regeneration that occurred within two months, the central TRPV1 expressing nerve terminals did not regenerate even after five months. The present study demonstrates that TRPV1 in the peripheral and central terminals play a role in nociception and the peripheral terminals have the ability to regenerate, whereas the central terminals do not regenerate even after five months.

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Section: Discussionmentioning

confidence: 99%

Section: Transient Receptor Potential Vanilloid 1 (Trpv1) Is a Camentioning

confidence: 99%

Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Yu¹,

Premkumar²

2015

TOPAINJ

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“…During each 2-minute observation period, scoring was done at 5-s intervals by an investigator who was blinded to the experimental groupings. The spontaneous pain index for each observation period was calculated by multiplying the interval number by the interval score and dividing by the total number of intervals (25 in all/session) (80). The overall pain index for each mouse on each day was obtained by averaging the scores obtained during the 3 observation periods.…”

Section: Antibodies and Reagents Taqman Primers And Probes For Rat Cmentioning

confidence: 99%

A shed form of LDL receptor–related protein–1 regulates peripheral nerve injury and neuropathic pain in rodents

Gaultier

Arandjelovic

et al. 2008

J. Clin. Invest.

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Injury to the peripheral nervous system (PNS) initiates a response controlled by multiple extracellular mediators, many of which contribute to the development of neuropathic pain. Schwann cells in an injured nerve demonstrate increased expression of LDL receptor-related protein-1 (LRP1), an endocytic receptor for diverse ligands and a cell survival factor. Here we report that a fragment of LRP1, in which a soluble or shed form of LRP1 with an intact α-chain (sLRP-α), was shed by Schwann cells in vitro and in the PNS after injury. Injection of purified sLRP-α into mouse sciatic nerves prior to chronic constriction injury (CCI) inhibited p38 MAPK activation (P-p38) and decreased expression of TNF-α and IL-1β locally. sLRP-α also inhibited CCI-induced spontaneous neuropathic pain and decreased inflammatory cytokine expression in the spinal dorsal horn, where neuropathic pain processing occurs. In cultures of Schwann cells, astrocytes, and microglia, sLRP-α inhibited TNF-α-induced activation of p38 MAPK and ERK/MAPK. The activity of sLRP-α did not involve TNF-α binding, but rather glial cell preconditioning, so that the subsequent response to TNF-α was inhibited. Our results show that sLRP-α is biologically active and may attenuate neuropathic pain. In the PNS, the function of LRP1 may reflect the integrated activities of the membrane-anchored and shed forms of LRP1.

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“…Recently, leptin has emerged as a modulator of inflammation and immune responses in the nervous system. The underlying mechanism is likely to be leptin-stimulated production of inflammatory mediators (8)(9)(10), which are also accepted molecular substrates for neuropathic pain (11)(12)(13). The present study focused on the role of leptin secreted from adipocytes in the PNS in neuropathic pain.…”

mentioning

confidence: 99%

“…Here, we show that tactile allodynia induced by partial sciatic nerve ligation is affected in its developmental phase by leptin possibly secreted from adipocytes in the epineurium of the sciatic nerve (SCN). Furthermore, the leptin signaling molecules involved in this regulation include some conventional molecular substrates for allodynia (11)(12)(13) produced by macrophages through activation of the JAK-STAT pathway.…”

mentioning

confidence: 99%

Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation

Maeda

Kiguchi

Kobayashi

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

103

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Nerve injury may result in neuropathic pain, characterized by allodynia and hyperalgesia. Accumulating evidence suggests the existence of a molecular substrate for neuropathic pain produced by neurons, glia, and immune cells. Here, we show that leptin, an adipokine exclusively produced by adipocytes, is critical for the development of tactile allodynia through macrophage activation in mice with partial sciatic nerve ligation (PSL). PSL increased leptin expression in adipocytes distributed at the epineurium of the injured sciatic nerve (SCN). Leptin-deficient animals, ob/ob mice, showed an absence of PSL-induced tactile allodynia, which was reversed by the administration of leptin to the injured SCN. Perineural injection of a neutralizing antibody against leptin reproduced this attenuation. Macrophages recruited to the perineurium of the SCN expressed the leptin receptor and phosphorylated signal transducer and activator of transcription 3 (pSTAT3), a transcription factor downstream of leptin. PSL also up-regulated the accepted mediators of neuropathic pain-namely, cyclooxygenase-2, inducible nitric oxide synthase, and matrix metalloprotease-9 -in the injured SCN, with transcriptional activation of their gene promoters by pSTAT3. This up-regulation was partly reproduced in a macrophage cell line treated with leptin. Administration of peritoneal macrophages treated with leptin to the injured SCN reversed the failure of ob/ob mice to develop PSLinduced tactile allodynia. We suggest that leptin induces recruited macrophages to produce pronociceptive mediators for the development of tactile allodynia. This report shows that adipocytes associated with primary afferent neurons may be involved in the development of neuropathic pain through adipokine secretion.adipokine ͉ allodynia ͉ C/EBP ͉ fat ͉ STAT

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

Cited by 122 publications

References 62 publications

Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

A shed form of LDL receptor–related protein–1 regulates peripheral nerve injury and neuropathic pain in rodents

Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation

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