ArticleInternational journal of molecular sciences2019
Myelination in Multiple Sclerosis Lesions Is Associated with Regulation of Bone Morphogenetic Protein 4 and Its Antagonist Noggin.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Noggin alleviates neuropathic pain by regulating microglial polarization and remodeling iron homeostasis via a STAT3-dependent pathway.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- An overview on microglial origin, distribution, and phenotype in Alzheimer's disease.Journal of cellular physiology · 2024Review
- Transient Receptor Potential Vanilloid 4-Dependent Microglial Function in Myelin Injury and Repair.International journal of molecular sciences · 2023Article
- Immunological dimensions of neuroinflammation and microglial activation: exploring innovative immunomodulatory approaches to mitigate neuroinflammatory progression.Frontiers in immunology · 2023Review
- Infiltrating circulating monocytes provide an important source of BMP4 at the early stage of spinal cord injury.Disease models & mechanisms · 2023Article
- Developmental Cues and Molecular Drivers in Myelinogenesis: Revisiting Early Life to Re-Evaluate the Integrity of CNS Myelin.Current issues in molecular biology · 2022Review
- The Role of Bone Morphogenetic Protein 4 in Microglial Polarization in the Process of Neuropathic Pain.Journal of inflammation research · 2022Article
- Regenerative Effects of CDP-Choline: A Dose-Dependent Study in the Toxic Cuprizone Model of De- and Remyelination.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Endothelial Nitric Oxide Synthase-Deficient Mice: A Model of Spontaneous Cerebral Small-Vessel Disease.The American journal of pathology · 2021Review
- The Wnt Effector TCF7l2 Promotes Oligodendroglial Differentiation by Repressing Autocrine BMP4-Mediated Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Acute Response and Neuroprotective Role of Myo/Nog Cells Assessed in a Rat Model of Focal Brain Injury.Frontiers in neuroscience · 2021Article
- MicroRNA profiles of MS gray matter lesions identify modulators of the synaptic protein synaptotagmin-7.Brain pathology (Zurich, Switzerland) · 2020Article
- Inhibitors of Myelination and Remyelination, Bone Morphogenetic Proteins, are Upregulated in Human Neurological Disease.Neurochemical research · 2020Review
- Microglia in Multiple Sclerosis: Friend or Foe?Frontiers in immunology · 2020Review
- Combinatory Multifactor Treatment Effects on Primary Nanofiber Oligodendrocyte Cultures.Cells · 2019Article
- CD8Multiple sclerosis journal - experimental, translational and clinicalArticle
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Remyelination is a central aspect of new multiple sclerosis (MS) therapies, in which one aims to alleviate disease symptoms by improving axonal protection. However, a central problem is mediators expressed in MS lesions that prevent effective remyelination. Bone morphogenetic protein4 (BMP4) inhibits the development of mature oligodendrocytes in cell culture and also blocks the expression of myelin proteins. Additionally, numerous studies have shown that Noggin (SYM1)-among other physiological antagonists of BMP4-plays a prominent role in myelin formation in the developing but also the adult central nervous system. Nonetheless, neither BMP4 nor Noggin have been systematically studied in human MS lesions. In this study, we demonstrated by transcript analysis and immunohistochemistry that BMP4 is expressed by astrocytes and microglia/macrophages in association with inflammatory infiltrates in MS lesions, and that astrocytes also express BMP4 in chronic inactive lesions that failed to remyelinate. Furthermore, the demonstration of an increased expression of Noggin in so-called shadow plaques (i.e., remyelinated lesions with thinner myelin sheaths) in comparison to chronically inactive demyelinated lesions implies that antagonizing BMP4 is associated with successful remyelination in MS plaques in humans. However, although BMP4 is strongly overexpressed in inflammatory lesion areas, its levels are also elevated in remyelinated lesion areas, which raises the possibility that BMP4 signaling itself may be required for remyelination. Therefore, remyelination might be influenced by a small number of key factors. Manipulating these molecules, i.e., BMP4 and Noggin, could be a promising therapeutic approach for effective remyelination.
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Registered trials
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