ArticleThe American journal of pathology2009
Matrix metalloproteinase-12 deficiency worsens relapsing-remitting experimental autoimmune encephalomyelitis in association with cytokine and chemokine dysregulation.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
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- Aging-Exacerbated Acute Axon and Myelin Injury Is Associated with Microglia-Derived Reactive Oxygen Species and Is Alleviated by the Generic Medication Indapamide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- NAD+ attenuates experimental autoimmune encephalomyelitis through induction of CD11b+ gr-1+ myeloid-derived suppressor cells.Bioscience reports · 2020Article
- Matrix metalloproteinases in the CNS: interferons get nervous.Cellular and molecular life sciences : CMLS · 2019Review
- Transcriptional networks of progressive diabetic peripheral neuropathy in the db/db mouse model of type 2 diabetes: An inflammatory story.Experimental neurology · 2018Article
- Caspase-1 inhibition prevents glial inflammasome activation and pyroptosis in models of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- C-terminal truncation of IFN-γ inhibits proinflammatory macrophage responses and is deficient in autoimmune disease.Nature communications · 2018Article
- Chondroitin sulfate proteoglycans as novel drivers of leucocyte infiltration in multiple sclerosis.Brain : a journal of neurology · 2018Article
- Systematic screening of generic drugs for progressive multiple sclerosis identifies clomipramine as a promising therapeutic.Nature communications · 2017Article
- Prolactin in combination with interferon-β reduces disease severity in an animal model of multiple sclerosis.Journal of neuroinflammation · 2015Article
- Stimulation of monocytes, macrophages, and microglia by amphotericin B and macrophage colony-stimulating factor promotes remyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Laquinimod reduces neuroaxonal injury through inhibiting microglial activation.Annals of clinical and translational neurology · 2014Article
- Relationship between metalloproteinase 2 and 9 concentrations and soluble CD154 expression in Iranian patients with multiple sclerosis.The Kaohsiung journal of medical sciences · 2014Article
- Reduction of microglial activity in a model of multiple sclerosis by dipyridamole.Journal of neuroinflammation · 2013Article
- Neural functions of matrix metalloproteinases: plasticity, neurogenesis, and disease.Biochemistry research international · 2012Article
- Predominance of Th2 polarization by vitamin D through a STAT6-dependent mechanism.Journal of neuroinflammation · 2011Article
- Minocycline prevents osmotic demyelination syndrome by inhibiting the activation of microglia.Journal of the American Society of Nephrology : JASN · 2010Article
- Cleavage of osteopontin by matrix metalloproteinase-12 modulates experimental autoimmune encephalomyelitis disease in C57BL/6 mice.The American journal of pathology · 2010Article
- Matrix metalloproteinases, synaptic injury, and multiple sclerosis.Frontiers in psychiatry · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The elevation of several members of the matrix metalloproteinase (MMP) family promotes the pathophysiology of both multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Nonetheless, given the multiple activities of MMPs, it remains possible that increased levels of a particular MMP may have beneficial functions during disease progression. We reported previously that MMP-12(-/-) mice of the 129/SvEv strain had a poorer EAE outcome than wild-type controls. However, we did not determine further differences in disease profiles between these groups. Using the EAE model in 129/SvEv mice, we report that disease in both wild-type and MMP-12(-/-) mice follows a relapsing-remitting course. Although both mouse groups had similar clinical onsets, subsequent relapses were more severe in MMP-12(-/-) mice; their residual disability at remission was also higher compared with wild-type controls. The worsened relapses and remissions in MMP-12(-/-) mice occurred despite a deficiency of the antigen recall capacity of lymph node-derived cells as well as a reduction in the proportion of macrophages in the spinal cord during the chronic phase of EAE. Significantly, large increases of levels of chemokines and cytokines were found in the spinal cords of MMP-12(-/-) mice during chronic EAE. These results highlight MMP-12 as a beneficial enzyme in EAE and suggest that therapeutic interventions in multiple sclerosis should avoid targeting MMP-12.
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