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Metalloproteinase MT5-MMP is an essential modulator of neuro-immune interactions in thermal pain stimulation
Abstract
Peripheral interactions between nociceptive fibers and mast cells contribute to inflammatory pain, but little is known about mechanisms mediating neuro-immune communication. Here we show that metalloproteinase MT5-MMP (MMP-24) is an essential mediator of peripheral thermal nociception and inflammatory hyperalgesia. We report that MT5-MMP is expressed by CGRP-containing peptidergic nociceptors in dorsal root ganglia and that Mmp24-deficient mice display enhanced sensitivity to noxious thermal stimuli under basal conditions. Consistently, mutant peptidergic sensory neurons hyperinnervate the skin, a phenotype that correlates with changes in the regulated cleavage of the cell-cell adhesion molecule N-cadherin. In contrast to basal nociception, Mmp24 −/− mice do not develop thermal hyperalgesia during inflammation, a phenotype that appears associated with alterations in N-cadherin-mediated cell-cell interactions between mast cells and sensory fibers. Collectively, our findings demonstrate an essential role of MT5-MMP in the development of dermal neuro-immune synapses and suggest that this metalloproteinase may be a target for pain control.
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Deficient cleavage of N-cadherin in the PNS was reported as a possible mechanism explaining the lack of inflammatory response to IL-1β injection in MT5-MMP-deficient mice.
“deficient cleavage of N-cadherin in the PNS was reported as a possible mechanism explaining the lack of inflammatory response to IL-1β injection in MT5-MMP-deficient mice [10]”
MT5-MMP deficiency prevents interleukin-1 beta (IL-1β)-mediated inflammation in the peripheral nervous system.
“MT5-MMP deficiency prevents interleukin-1 beta (IL-1β)-mediated inflammation in the peripheral nervous system.”
In MT5-MMP-deficient mice, MT5-MMP deficiency prevents proper N-cadherin processing, eventually disrupting the crosstalk between sensory neurons and mast cells.
“MT5-MMP-deficient prevented proper N-cadherin processing eventually disrupting the crosstalk between sensory neurons and mast cells [10].”
Systemic injection of IL-1β does not trigger an inflammatory response in the PNS of adult MT5-MMP-deficient mice.
“systemic injection of IL-1β did not trigger an inflammatory response in the PNS of adult MT5-MMP-deficient mice [10].”
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Metadata
- Authors
- Folgueras, A. R., Valdés-Sánchez, T., Llano, E., Menéndez, L., Baamonde, A., Denlinger, B. L., Belmonte, C., Juárez, L., Lastra, A., García-Suárez, O., Astudillo, A., Kirstein, M., Pendás, A. M., Fariñas, I., & López-Otín, C.
- Affiliations
- Departamento de Bioquímica y Biología Molecular and
- Departamento de Biología Celular and Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas, Universidad de Valencia, 46100-Burjassot, Spain;
- Laboratorio de Farmacología, Facultad de Medicina, Instituto Universitario de Oncología, Universidad de Oviedo, 33006-Oviedo, Spain;
- Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas, 03550-San Juan de Alicante, Spain; and
- Servicio de Anatomía Patológica, Hospital Central de Asturias, 33006-Oviedo, Spain
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-09-22
- Volume
- 106
- Issue
- 38
- Pages
- 16451-16456
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 80
- References
- 2
- Language
- en
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