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MMP 7 cleaves remyelination‐impairing fibronectin aggregates and its expression is reduced in chronic multiple sclerosis lesions
Abstract
Upon demyelination, transient expression of fibronectin precedes successful remyelination. However, in chronic demyelination observed in multiple sclerosis (MS), aggregates of fibronectin persist and contribute to remyelination failure. Accordingly, removing fibronectin (aggregates) would constitute an effective strategy for promoting remyelination. Matrix metalloproteinases (MMPs) are enzymes known to remodel extracellular matrix components, including fibronectin. Here, we examined the ability of MMPs to degrade fibronectin aggregates. Our findings reveal that MMP7 cleaved fibronectin aggregates resulting into a prominent 13 kDa EIIIA (16 kDa EDA)‐containing fragment. MMP7 was upregulated during lysolecithin‐induced demyelination, indicating its potential for endogenous fibronectin clearance. In contrast, the expression of proMMP7 was substantially decreased in chronic active and inactive MS lesions compared with control white matter and remyelinated MS lesions. Microglia and macrophages were major cellular sources of proMMP7 and IL‐4‐activated, but not IFNγ+LPS‐activated, microglia and macrophages secreted significant levels of proMMP7. Also, conditioned medium of IL‐4‐activated macrophages most efficiently cleaved fibronectin aggregates upon MMP‐activating conditions. Yet, coatings of MMP7‐cleaved fibronectin aggregate fragments inhibited oligodendrocyte maturation, indicating that further degradation and/or clearance by phagocytosis is essential. These findings suggest that MMP7 cleaves fibronectin aggregates, while reduced (pro)MMP7 levels in MS lesions contribute to their persistent presence. Therefore, upregulating MMP7 levels may be key to remove remyelination‐impairing fibronectin aggregates in MS lesions.
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MMP7 participates in the removal of neuronal myelinization, protecting against fibronectin aggregates in multiple sclerosis lesions.
“and in the removal of neuronal myelinization, protecting against fibronectin aggregates in multiple sclerosis lesions.57”
From Canonical Wnt pathway and the LDL receptor superfamily in neuronal cholesterol homeostasis and function (2024) · cites this paper as [57]
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Extracellular Matrix Degradation and Remodeling in Development and Disease
Lu, P., Takai, K., Weaver, V. M., & Werb, Z. (2011) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a005058 · Cited by 2,265
M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination
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Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity
Fünfschilling, U., Supplie, L. M., Mahad, D., Boretius, S., Saab, A. S., Edgar, J., Brinkmann, B. G., Kassmann, C. M., Tzvetanova, I. D., Möbius, W., et al. (2012) · Nature · doi:10.1038/nature11007 · Cited by 1,523
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Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation
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Macrophages in inflammatory multiple sclerosis lesions have an intermediate activation status
Vogel, D. Y., Vereyken, E. J., Glim, J. E., Heijnen, P. D., Moeton, M., van der Valk, P., Amor, S., Teunissen, C. E., van Horssen, J., & Dijkstra, C. D. (2013) · Journal of Neuroinflammation · doi:10.1186/1742-2094-10-35 · Cited by 479
Self-citationGlial response during cuprizone-induced de- and remyelination in the CNS: lessons learned
Gudi, V., Gingele, S., Skripuletz, T., & Stangel, M. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00073 · Cited by 375
Cortical remyelination: A new target for repair therapies in multiple sclerosis
Chang, A., Staugaitis, S. M., Dutta, R., Batt, C. E., Easley, K. E., Chomyk, A. M., Yong, V. W., Fox, R. J., Kidd, G. J., & Trapp, B. D. (2012) · Annals of Neurology · doi:10.1002/ana.23693 · Cited by 216
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“Coincidentally, mRNA levels of TIMP1, a natural inhibitor of MMPs, were substantially increased at demyelination, and decreased at remyelination (14 DPL) compared with 5 DPL (Figure 1a).”
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Borrell-Pages, M., Luquero, A., Vilahur, G., Padró, T., & Badimon, L. (2024) · Cardiovascular Research · doi:10.1093/cvr/cvad159 · Cited by 10
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Metadata
- Authors
- Wang, P., Gorter, R. P., de Jonge, J. C., Nazmuddin, M., Zhao, C., Amor, S., Hoekstra, D., & Baron, W.
- Affiliations
- Department of Cell Biology University of Groningen, University Medical Center Groningen Groningen the Netherlands
- Wellcome Trust – Medical Research Council Cambridge Stem Cell Institute and Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom
- Department of Pathology VU Medical Center Amsterdam the Netherlands
- ORCID
- Baron, Wia
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2018-03-30
- Volume
- 66
- Issue
- 8
- Pages
- 1625-1643
- ISSN
- 0894-1491
- 1098-1136
- PMC
- PMC6099312
- Cited by
- 40
- References
- 12
- Language
- en
- Funders
- Stichting MS Research
- China Scholarship Council
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