ArticleProceedings of the National Academy of Sciences of the United States of America1995
Insulin-like growth factor I treatment reduces demyelination and up-regulates gene expression of myelin-related proteins in experimental autoimmune encephalomyelitis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 210 citations in OpenAlex.
- Review
- Neuroprotective Effects of VEGF-B in a Murine Model of Aggressive Neuronal Loss with Childhood Onset.International journal of molecular sciences · 2025Article
- Insulin-like growth factor-1 receptor controls the function of CNS-resident macrophages and their contribution to neuroinflammation.Acta neuropathologica communications · 2023Article
- Neurotrophic Factors as Regenerative Therapy for Neurodegenerative Diseases: Current Status, Challenges and Future Perspectives.International journal of molecular sciences · 2023Review
- Platelet-rich plasma loaded nerve guidance conduit as implantable biocompatible materials for recurrent laryngeal nerve regeneration.NPJ Regenerative medicine · 2022Article
- Newly Identified Deficiencies in the Multiple Sclerosis Central Nervous System and Their Impact on the Remyelination Failure.Biomedicines · 2022Review
- Hormones in experimental autoimmune encephalomyelitis (EAE) animal models.Translational neuroscience · 2021Review
- Growth Factors and Their Roles in Multiple Sclerosis Risk.Frontiers in immunology · 2021Article
- Beneficial Roles of Microglia and Growth Factors in MS, a Brief Review.Frontiers in cellular neuroscience · 2020Review
- Dynamic response of microglia/macrophage polarization following demyelination in mice.Journal of neuroinflammation · 2019Article
- Umbilical cord blood versus mesenchymal stem cells for inflammation-induced preterm brain injury in fetal sheep.Pediatric research · 2019Article
- The role of glial-neuronal metabolic cooperation in modulating progression of multiple sclerosis and neuropathic pain.Immunotherapy · 2019Review
- IGFBP-2 Signaling in the Brain: From Brain Development to Higher Order Brain Functions.Frontiers in endocrinology · 2019Review
- Insulin resistance and exendin-4 treatment for multiple system atrophy.Brain : a journal of neurology · 2017Article
- The role of growth factors as a therapeutic approach to demyelinating disease.Experimental neurology · 2016Review
- Extracellular cues influencing oligodendrocyte differentiation and (re)myelination.Experimental neurology · 2016Review
- Depletion of Olig2 in oligodendrocyte progenitor cells infected by Theiler's murine encephalomyelitis virus.Journal of neurovirology · 2016Article
- Trophic factors intervention regenerates the nestin-expressing cell population in a model of perinatal excitotoxicity: Implications for perinatal brain injury and prematurity.Integrative molecular medicine · 2016Article
- Glia Disease and Repair-Remyelination.Cold Spring Harbor perspectives in biology · 2015Review
- Insulin-like growth factor-1 stimulates regulatory T cells and suppresses autoimmune disease.EMBO molecular medicine · 2014Article
4 more citing papers are in PubMed but not listed here.
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4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To compare effects of insulin-like growth factor I (IGF-I) and placebo treatment on lesions that resemble those seen during active demyelination in multiple sclerosis, we induced experimental autoimmune encephalomyelitis in Lewis rats with an emulsion containing guinea pig spinal cord and Freund's adjuvant. On day 12-13, pairs of rats with the same degree of weakness were given either IGF-I or placebo intravenously twice daily for 8 days. After 8 days of placebo or IGF-I (200 micrograms/day or 1 mg/day) treatment, the spinal cord lesions were studied by in situ hybridization and with immunocytochemical and morphological methods. IGF-I produced significant reductions in numbers and areas of demyelinating lesions. These lesions contained axons surrounded by regenerating myelin segments instead of demyelinated axons seen in the placebo-treated rats. Relative mRNA levels for myelin basic protein, proteolipid protein (PLP), and 2',3'-cyclic nucleotide 3'-phosphodiesterase in lesions of IGF-I-treated rats were significantly higher than they were in placebo-treated rats. PLP mRNA-containing oligodendroglia also were more numerous and relative PLP mRNA levels per oligodendrocyte were higher in lesions of IGF-I-treated rats. Finally, a significantly higher proportion of proliferating cells were oligodendroglia-like cells in lesions of IGF-I-treated rats. We think that IGF-I effects on oligodendrocytes, myelin protein synthesis, and myelin regeneration reduced lesion severity and promoted clinical recovery in this experimental autoimmune encephalomyelitis model. These IGF-I actions may also benefit patients with multiple sclerosis.
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