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Updated: Jul 12, 2026
Implanting Glass Spinal Cord Windows in Adult Mice with Experimental Autoimmune Encephalomyelitis
Published on: December 21, 2013
Bone morphogenetic proteins 4, 6, and 7 are up-regulated in mouse spinal cord during experimental autoimmune
Jahan Ara1, Jill See, Polina Mamontov
1Department of Pediatrics, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA.
Abstract:
Although spontaneous remyelination occurs in multiple sclerosis (MS), the extent of myelin repair is often inadequate to restore normal function. Oligodendrocyte precursors remaining in nonremyelinating MS plaques may be restricted by an inhibitory signal. Bone morphogenetic proteins (BMPs) have been implicated as repressors of oligodendrocyte development and inducers of astrogliogenesis. We hypothesized that BMPs are up-regulated in MS lesions and play a role in demyelination and astrogliosis. We examined expression of BMPs in an animal model of MS, chronic experimental autoimmune encephalomyelitis (EAE) induced by the myelin oligodendrocyte glycoprotein (MOG) peptide in C57BL/6 mice. By 14 days postimmunization, compared to those of control mice, the lumbar spinal cords of MOG-peptide EAE mice demonstrated prominent astrogliosis, infiltration of inflammatory cells, and disrupted expression of myelin proteins. Quantitative RT-PCR showed that expression of BMP4, BMP6, and BMP7 mRNA increased 2- to 4-fold in the lumbar spinal cords of animals with symptomatic EAE versus in vehicle-treated and untreated controls on days 14, 21, and 42 postimmunization. BMP2 mRNA expression was not altered. BMP4 mRNA was much more abundant in the spinal cords of all animals than was mRNA encoding BMP2, BMP6, and BMP7. Immunoblot analysis confirmed the increased expression of BMP4 in the EAE animals. Immunohistochemistry revealed increased BMP4 immunoreactivity in areas of inflammation in MOG-peptide EAE animals. BMP4 labeling was mostly limited to macrophages but was sometimes associated with astrocytes and oligodendrocytes. These results indicate that members of the BMP family are differentially expressed in adult spinal cord and are up-regulated during EAE. (c) 2007 Wiley-Liss, Inc.
Insights
Bone morphogenetic proteins (BMPs) are elevated in multiple sclerosis (MS) lesions, potentially hindering myelin repair. This study found increased BMP4 expression in an MS animal model, suggesting BMPs contribute to disease pathology.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Spontaneous remyelination in multiple sclerosis (MS) is often insufficient for functional recovery.
- Oligodendrocyte precursor cells in MS plaques may be inhibited by specific signals.
- Bone morphogenetic proteins (BMPs) are known to inhibit oligodendrocyte development and promote astrocyte formation.
Purpose of the Study:
- To investigate the role of BMPs in MS pathology.
- To determine if BMPs are upregulated in MS lesions.
- To explore the potential involvement of BMPs in demyelination and astrogliosis.
Main Methods:
- Utilized a mouse model of MS (chronic experimental autoimmune encephalomyelitis - EAE) induced by myelin oligodendrocyte glycoprotein (MOG) peptide.
- Analyzed lumbar spinal cord tissue from EAE mice and control groups.
- Employed quantitative RT-PCR, immunoblot analysis, and immunohistochemistry to assess BMP expression and localization.
Main Results:
- EAE mice exhibited significant astrogliosis, inflammation, and disrupted myelin protein expression.
- Expression of BMP4, BMP6, and BMP7 mRNA was significantly increased (2- to 4-fold) in EAE mice compared to controls.
- BMP4 mRNA was the most abundant BMP transcript, and increased BMP4 protein levels and immunoreactivity were confirmed in inflamed areas of EAE spinal cords, localized to macrophages, astrocytes, and oligodendrocytes.
Conclusions:
- BMP family members show differential expression in the adult spinal cord.
- BMPs, particularly BMP4, are upregulated during experimental autoimmune encephalomyelitis (EAE).
- These findings suggest that upregulated BMPs may play a role in the demyelination and astrogliosis observed in MS.
