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      Matrix Metalloproteinases in Neuropathic Pain and Migraine: Friends, Enemies, and Therapeutic Targets

      review-article
      Author(s): 1 , * , 1 , 2
      Publication date (Electronic):
      Journal: Pain Research and Treatment
      Publisher: Hindawi Publishing Corporation

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          Abstract

          Matrix metalloproteinases (MMPs) constitute a family of zinc-dependent endopeptidases that mediate extracellular matrix turnover and associated processes, such as cell survival, growth, and differentiation. This paper discusses important functions of MMP in the normal and injured nervous system, focusing on the role played by these proteases in neurological pain syndromes, most prominently in neuropathic pain and migraine headaches. In the past decade, metalloproteinases emerged as key modulators of neuropathic pain, with MMP-9 acting as an initiator of the neuropathic cascade. Increased MMP activity was detected in migraine patients, independent of aura, in tight association with metabolic derangements. The therapeutic implications of MMP inhibition are considered in the context of neurogenic pain regulation.

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          ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model.

          Zhi-Ye Zhuang, Peter Gerner, Clifford Woolf … (2005)
          Activation of extracellular signal-regulated kinase (ERK), a mitogen activated-protein kinase (MAPK), in dorsal horn neurons contributes to inflammatory pain by transcription-dependent and -independent means. We have now investigated if ERK is activated in the spinal cord after a spinal nerve ligation (SNL) and if this contributes to the neuropathic pain-like behavior generated in this model. An L5 SNL induces an immediate (<10 min) but transient (<6 h) induction of phosphoERK (pERK) restricted to neurons in the superficial dorsal horn. This is followed by a widespread induction of pERK in spinal microglia that peaks between 1 and 3 days post-surgery. On Day 10, pERK is expressed both in astrocytes and microglia, but by Day 21 predominantly in astrocytes in the dorsal horn. In the L5 DRG SNL transiently induces pERK in neurons at 10 min, and in satellite cells on Day 10 and 21. Intrathecal injection of the MEK (ERK kinase) inhibitor PD98059 on Day 2, 10 or 21 reduces SNL-induced mechanical allodynia. Our results suggest that ERK activation in the dorsal horn, as well as in the DRG, mediates pain through different mechanisms operating in different cells at different times. The sequential activation of ERK in dorsal horn microglia and then in astrocytes might reflect distinct roles for these two subtypes of glia in the temporal evolution of neuropathic pain.
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            Recent findings on how proinflammatory cytokines cause pain: peripheral mechanisms in inflammatory and neuropathic hyperalgesia.

            Claudia Sommer, Michaela Kress (2004)
            Numerous experimental studies provide evidence that proinflammatory cytokines induce or facilitate inflammatory as well as neuropathic pain and hyperalgesia. Direct receptor-mediated actions of cytokines on afferent nerve fibers have been reported as well as cytokine effects involving further mediators. The final outcome of cytokine action greatly depends on whether they act in the central of in the peripheral nervous system. Here we summarize recent findings on the peripheral mechanisms of action of three prototypic proinflammatory cytokines, interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha, with regards to pain and hyperalgesia.
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              Role of matrix metalloproteinases in delayed cortical responses after stroke.

              Bing-Qiao Zhao, Sophia Wang, Hahn-Young Kim … (2006)
              Matrix metalloproteinases (MMPs) are zinc-endopeptidases with multifactorial actions in central nervous system (CNS) physiology and pathology. Accumulating data suggest that MMPs have a deleterious role in stroke. By degrading neurovascular matrix, MMPs promote injury of the blood-brain barrier, edema and hemorrhage. By disrupting cell-matrix signaling and homeostasis, MMPs trigger brain cell death. Hence, there is a movement toward the development of MMP inhibitors for acute stroke therapy. But MMPs may have a different role during delayed phases after stroke. Because MMPs modulate brain matrix, they may mediate beneficial plasticity and remodeling during stroke recovery. Here, we show that MMPs participate in delayed cortical responses after focal cerebral ischemia in rats. MMP-9 is upregulated in peri-infarct cortex at 7-14 days after stroke and is colocalized with markers of neurovascular remodeling. Treatment with MMP inhibitors at 7 days after stroke suppresses neurovascular remodeling, increases ischemic brain injury and impairs functional recovery at 14 days. MMP processing of bioavailable VEGF may be involved because inhibition of MMPs reduces endogenous VEGF signals, whereas additional treatment with exogenous VEGF prevents MMP inhibitor-induced worsening of infarction. These data suggest that, contrary to MMP inhibitor therapies for acute stroke, strategies that modulate MMPs may be needed for promoting stroke recovery.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Pain Res Treat
                Journal ID (iso-abbrev): Pain Res Treat
                Journal ID (publisher-id): PRT
                Title: Pain Research and Treatment
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-1542
                ISSN (Electronic): 2090-1550
                Publication date (Print): 2012
                Publication date (Electronic): 28 August 2012
                Volume: 2012
                Electronic Location Identifier: 952906
                Affiliations
                1Global Neuroscience Initiative Foundation, Los Angeles, CA 90210, USA
                2Verland Medical Communications, Pittsburg, PA 15201, USA
                Author notes
                *Shaheen E. Lakhan: slakhan@ 123456gnif.org

                Academic Editor: Jonathan O. Dostrovsky

                Article
                DOI: 10.1155/2012/952906
                PMC ID: 3434407
                PubMed ID: 22970361
                SO-VID: e437502c-f096-489c-9233-eccd7590df8b
                Copyright © Copyright © 2012 S. E. Lakhan and M. Avramut.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 May 2012
                Date revision received : 13 July 2012
                Date accepted : 16 July 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Anesthesiology & Pain management
                Data availability:
                ScienceOpen disciplines: Anesthesiology & Pain management

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