Specific matrix metalloproteinase 9 (MMP-9) haplotype affect the circulating MMP-9 levels in women with migraine

Martins-Oliveira, Alisson; Gonçalves, Flavia M.; Speciali, José Geraldo; Fontana, Vanessa; Izidoro-Toledo, Tatiane C.; Belo, Vanessa A.; Dach, Fabíola; Tanus‐Santos, Jose E.

doi:10.1016/j.jneuroim.2012.07.016

Cited by 21 publications

(14 citation statements)

References 42 publications

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“…Furthermore, Martins‐Oliveira et al . () found that combinations of MMP‐9 gene polymorphisms affected circulating MMP‐9 levels and that high MMP‐9 concentrations in patients with migraine were associated with a specific MMP‐9 haplotype.…”

Section: Pathologies: Predisposition Diagnosis and Therapy (Animal mentioning

confidence: 99%

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Vafadari

Salamian

Kaczmarek

2016

Journal of Neurochemistry

310

257

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Matrix metalloproteinase-9 (MMP-9) is a member of the metzincin family of mostly extracellularly operating proteases. Despite the fact that all of these enzymes might be target promiscuous, with largely overlapping catalogs of potential substrates, MMP-9 has recently emerged as a major and apparently unique player in brain physiology and pathology. The specificity of MMP-9 may arise from its very local and time-restricted actions, even when released in the brain from cells of various types, including neurons, glia, and leukocytes. In fact, the quantity of MMP-9 is very low in the naive brain, but it is markedly activated at the levels of enzymatic activity, protein abundance, and gene expression following various physiological stimuli and pathological insults. Neuronal MMP-9 participates in synaptic plasticity by controlling the shape of dendritic spines and function of excitatory synapses, thus playing a pivotal role in learning, memory, and cortical plasticity. When improperly unleashed, MMP-9 contributes to a large variety of brain disorders, including epilepsy, schizophrenia, autism spectrum disorder, brain injury, stroke, neurodegeneration, pain, brain tumors, etc. The foremost mechanism of action of MMP-9 in brain disorders appears to be its involvement in immune/inflammation responses that are related to the enzyme's ability to process and activate various cytokines and chemokines, as well as its contribution to bloodbrain barrier disruption, facilitating the extravasation of leukocytes into brain parenchyma. However, another emerging possibility (i.e., the control of MMP-9 over synaptic plasticity) should not be neglected. The translational potential of MMP-9 has already been recognized in both the diagnosis and treatment domains. The most striking translational aspect may be the discovery of MMP-9 up-regulation in a mouse model of Fragile X syndrome, quickly followed by human studies and promising clinical trials that have sought to inhibit MMP-9. With regard to diagnosis, suggestions have been made to use MMP-9 alone or combined with tissue inhibitor of matrix metalloproteinase-1 or brain-derived neurotrophic factor as disease biomarkers.

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Section: Pathologies: Predisposition Diagnosis and Therapy (Animal mentioning

confidence: 99%

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Vafadari

Salamian

Kaczmarek

2016

Journal of Neurochemistry

310

257

View full text Add to dashboard Cite

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“…107 MMP levels (MMP-2 and MMP-9) have been shown to be elevated post-TBI, 108 as well as in patients with migraine. 109,110 Cortical spreading depression, which has been described in stroke, head trauma, and migraine, 111 has been shown to upregulate MMP-9, with associated alterations in BBB permeability. 112 P2X 7 is a purinergic receptor on microglia activated by extracellular neuron-derived ATP that is implicated in the induction and maintenance of both neuropathic and inflammatory pain by modulating the release of cytokines that sensitize sensory nerve terminals; 113,114 P2X 7 plays a particularly important role in the release of IL-1β.…”

Section: Brain Injury and Neuroinflammationmentioning

confidence: 99%

Traumatic Brain Injury, Neuroinflammation, and Post‐Traumatic Headaches

2013

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Concussions following head and/or neck injury are common, and although most people with mild injuries recover uneventfully, a subset of individuals develop persistent post-concussive symptoms that often include headaches. Post-traumatic headaches vary in presentation and may progress to become chronic and in some cases debilitating. Little is known about the pathogenesis of post-traumatic headaches, although shared pathophysiology with that of the brain injury is suspected. Following primary injury to brain tissues, inflammation rapidly ensues; while this inflammatory response initially provides a defensive/reparative function, it can persist beyond its beneficial effect, potentially leading to secondary injuries because of alterations in neuronal excitability, axonal integrity, central processing, and other changes. These changes may account for the neurological symptoms often observed after traumatic brain injury, including headaches. This review considers selected aspects of the inflammatory response following traumatic brain injury, with an emphasis on the role of glial cells as mediators of maladaptive post-traumatic inflammation.

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“…Some magnetic resonance imaging studies have reported negative results [126, 127] while others have found indications of BBB leakage [128]. In migraine, indirect evidence for BBB permeabilization is provided by increased circulating levels of matrix metalloproteinases (MMPs) 2 [129] and 9 [130] that have been attributed to MMPs release from the extracellular matrix of the neurovascular unit.…”

Section: Comorbidities Of Chronic Pain With Neuroinflammatory and mentioning

confidence: 99%

Neurovascular Unit in Chronic Pain

Radu

Bramantı

Osculati

et al. 2013

Mediators of Inflammation

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Chronic pain is a debilitating condition with major socioeconomic impact, whose neurobiological basis is still not clear. An involvement of the neurovascular unit (NVU) has been recently proposed. In particular, the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB), two NVU key players, may be affected during the development of chronic pain; in particular, transient permeabilization of the barrier is suggested by several inflammatory- and nerve-injury-based pain models, and we argue that the clarification of molecular BBB/BSCB permeabilization events will shed new light in understanding chronic pain mechanisms. Possible biases in experiments supporting this theory and its translational potentials are discussed. Moving beyond an exclusive focus on the role of the endothelium, we propose that our understanding of the mechanisms subserving chronic pain will benefit from the extension of research efforts to the NVU as a whole. In this view, the available evidence on the interaction between analgesic drugs and the NVU is here reviewed. Chronic pain comorbidities, such as neuroinflammatory and neurodegenerative diseases, are also discussed in view of NVU changes, together with innovative pharmacological solutions targeting NVU components in chronic pain treatment.

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Specific matrix metalloproteinase 9 (MMP-9) haplotype affect the circulating MMP-9 levels in women with migraine

Cited by 21 publications

References 42 publications

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

MMP‐9 in translation: from molecule to brain physiology, pathology, and therapy

Traumatic Brain Injury, Neuroinflammation, and Post‐Traumatic Headaches

Neurovascular Unit in Chronic Pain

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