Spatial and temporal analysis of nociception-related spinal cord matrix metalloproteinase expression in a murine neuropathic pain model

Liou, Jiin-Tarng; Sum, Daniel Ching-Wah; Liu, Fu-Chao; Mao, Chih-Chieh; Lai, Ying-Shu; Day, Yuan-Ji

doi:10.1016/j.jcma.2012.12.011

Cited by 22 publications

(17 citation statements)

References 44 publications

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“…Furthermore, intrathecal injection of MMP-2 caused neuropathic pain in mice, whilst peritoneal administration of GM6001, a general inhibitor of MMP, significantly attenuated thermal hyperalgesia and tactile allodynia induced by nerve injury. 23 Therefore, both MMP-9 and MMP-2 seem essential for the development and maintenance of chronic neuropathic pain, as these metalloproteinases are involved specifically in the initiation and the persistence of neuropathic pain, respectively.…”

Section: Matrix Metalloproteinase and Microglia Interactionmentioning

confidence: 99%

The role of microglia in the pathobiology of neuropathic pain development: what do we know?

Zhao

Alam

Chen

et al. 2017

British Journal of Anaesthesia

168

128

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Neuropathic pain, a maladaptive and chronic condition that can develop after a lesion or disease affecting the somatosensory system, is characterized by allodynia, hyperalgesia and spontaneous pain, and comorbidities such as sleep deprivation, depression and anxiety. The activation of microglial cells in response to nerve injury has been implicated in the development of neuropathic pain. Mediators such as Neuregulin-1, matrix metalloproteinase (MMP)-2, MMP-9, The chemokine (C-C motif) ligand 2 (CCL2) and fractalkine are released after nerve injury and are involved in the activation of microglial cells. These activated cells in turn release factors that increase the excitation and decrease the inhibition of interneurons. Microglial cells release factors such as interleukin (IL)-6, IL-1β and tumour necrosis factor-α (TNF-α) that cause the painful symptoms. It is becoming increasingly apparent that an intricate network of cytokines and cellular signalling mechanisms underpin the complex relationship between microglia and various cell types including neurones, astrocytes, oligodendrocytes, mast cells and T-cells. Although the precise mechanism of action of microglial cells in producing neuropathic pain has not been completely elucidated, research into these different activating factors and cytokines is providing further insight into the role of microglial cells in the development and maintenance of neuropathic pain. Further studies also are required to elucidate how "pain" mediators act on neurones and how the interactions between these mediators, or between neurones and glia in the presence of these mediators occur, in order to develop effective therapies for the management of neuropathic pain.

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Section: Matrix Metalloproteinase and Microglia Interactionmentioning

confidence: 99%

The role of microglia in the pathobiology of neuropathic pain development: what do we know?

Zhao

Alam

Chen

et al. 2017

British Journal of Anaesthesia

168

128

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“…In the next step, pro-inflammatory compounds such as metalloproteinases are produced, enzymes inducing connective tissue around nerves to expand and to become hyperactivated. 4 These initial steps are followed by activation of a number of pro-inflammatory cells, such as mast cells, macrophages, fibroblasts, neutrophils, and Schwann cells. 5 This leads to a release of various pro-inflammatory molecules: ATP, cytokines, CCL2, PGs, and various NGFs.…”

Section: Pathogenesis In Nerve Compression Syndromesmentioning

confidence: 99%

Palmitoylethanolamide, a neutraceutical, in nerve compression syndromes: efficacy and safety in sciatic pain and carpal tunnel syndrome

Hesselink

Kopsky

2015

JPR

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Palmitoylethanolamide (PEA) is an endogenous lipid modulator in animals and humans, and has been evaluated since the 1970s as an anti-inflammatory and analgesic drug in more than 30 clinical trials, in a total of ~6,000 patients. PEA is currently available worldwide as a nutraceutical in different formulations, with and without excipients. Here we describe the results of all clinical trials evaluating PEA’s efficacy and safety in nerve compression syndromes: sciatic pain and pain due to carpal tunnel syndrome, and review preclinical evidence in nerve impingement models. Both the pharmacological studies as well as the clinical trials supported PEA’s action as an analgesic compound. In total, eight clinical trials have been published in such entrapment syndromes, and 1,366 patients have been included in these trials. PEA proved to be effective and safe in nerve compression syndromes. In one pivotal, double blind, placebo controlled trial in 636 sciatic pain patients, the number needed to treat to reach 50% pain reduction compared to baseline was 1.5 after 3 weeks of treatment. Furthermore, no drug interactions or troublesome side effects have been described so far. Physicians are not always aware of PEA as a relevant and safe alternative to opioids and co-analgesics in the treatment of neuropathic pain. Especially since the often prescribed co-analgesic pregabaline has been proven to be ineffective in sciatic pain in a double blind enrichment trial, PEA should be considered as a new and safe treatment option for nerve compression syndromes.

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“…It suggests these proteolytic enzymes play a role in NP pathomechanism . Other studies conducted on animal models demonstrated rise in MMP‐2 and MMP‐9 activities in different phases of NP development . MMP‐9 showed rapid but short‐lasting upregulation (1–3 days) in the primary sensory neurons in the dorsal roots ganglions (DRG) after spinal nerve ligation in mice.…”

Section: Introductionmentioning

confidence: 99%

“…Different mechanisms of NP may contribute to a single disease entity in one patient and may be responsible for diversity of clinical manifestations . Studies on animal models demonstrated a role of metalloproteinases (MMPs), particularly MMP‐2 and MMP‐9, in pathomechanism of NP . MMPs act not only as mediators for neuroinflammation but may also be directly involved in evoking pain associated with nerve damage .…”

Section: Introductionmentioning

confidence: 99%

“…Their first recognized and most prominent function is cleaving the components of extracellular matrix . Activity of MMPs can be compromised by the action of four physiological tissue inhibitors of metalloproteinases (TIMPs) TIMP‐1, ‐2, ‐3, and ‐4 . MMP‐2 and MMP‐9 influence maturation of inflammatory cytokines modulating induction of neuroinflammation during development of NP .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Serum Level of Metalloproteinase-2 but not Metalloproteinase-9 Rises in Patients With Failed Back Surgery Syndrome After Spinal Cord Stimulation

Kamieniak

Bielewicz

Kurzepa

et al. 2019

Neuromodulation: Technology at the Neural Interface

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Spatial and temporal analysis of nociception-related spinal cord matrix metalloproteinase expression in a murine neuropathic pain model

Cited by 22 publications

References 44 publications

The role of microglia in the pathobiology of neuropathic pain development: what do we know?

The role of microglia in the pathobiology of neuropathic pain development: what do we know?

Palmitoylethanolamide, a neutraceutical, in nerve compression syndromes: efficacy and safety in sciatic pain and carpal tunnel syndrome

Serum Level of Metalloproteinase-2 but not Metalloproteinase-9 Rises in Patients With Failed Back Surgery Syndrome After Spinal Cord Stimulation

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