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Insulin-Like Growth Factor-1 Inhibits Mature Oligodendrocyte Apoptosis during Primary Demyelination
Open accessAbstract
Metabolic insult results in apoptosis and depletion of mature oligodendrocytes during demyelination. To examine the role of insulin-like growth factor-1 (IGF-1) during acute demyelination and remyelination in the adult CNS, we exposed transgenic mice that continuously express IGF-1 (IGF-1 tg) to cuprizone intoxication. Demyelination was observed within the corpus callosum in both wild-type and IGF-1 tg mice 3 weeks after exposure to cuprizone. Wild-type mice showed significant apoptotic mature oligodendrocytes and a dramatic loss of these cells within the lesion that resulted in near complete depletion and demyelination by week 5. In contrast, the demyelinated corpus callosum of the IGF-1 tg mice was near full recovery by week 5. This rapid recovery was apparently caused by survival of the mature oligodendrocyte population because apoptosis was negligible, and by week 4, the mature oligodendrocyte population was completely restored. Furthermore, despite demyelination in both wild-type and IGF-1 tg mice, oligodendrocyte progenitors accumulated only in the absence of mature oligodendrocytes and failed to accumulate if the mature oligodendrocytes remained as demonstrated in the IGF-1 tg mice. These results suggest that IGF-1 may be important in preventing the depletion of mature oligodendrocytes in vivo and thus facilitates an early recovery from demyelination.
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Surviving oligodendrocytes in IGF-1 over-expressing mice seem to retain the ability to remyelinate timely at week 5 regardless of remaining myelin debris.
“Moreover, these surviving oligodendrocytes even seem to retain the ability to remyelinate timely on week 5, regardless of remaining myelin debris (Mason et al., 2000b).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2000b
The Discussion (page unavailable) says that remyelination occurred at weeks 4 and 5 in IGF-1 transgenic mice and that surviving mature oligodendrocytes most likely contributed. The Early recovery section (page unavailable) reports substantial remyelination at week 5. Our copy does not establish that myelin debris remained or that remyelination occurred regardless of it. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIGF-1 over-expressing mice exhibited enhanced demyelination at week 3 but almost complete myelin recovery at week 5, in contrast to wild-type mice that had a severe myelin deficit at week 5.
“Additionally, these mice exhibited an enhanced demyelination at week 3 but an almost complete myelin recovery at week 5 in contrast to wt mice undergoing a severe myelin deficit at this time point.”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2000b
The ‘Early recovery from acute demyelination in IGF-1 tg mice’ section reports significant demyelination in both groups at week 3, followed by substantial remyelination in IGF-1 transgenic mice and nearly complete demyelination in wild-type mice at week 5. It does not support greater week-3 demyelination in the transgenic mice; it suggests their demyelinating insult was less extensive. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSJL mice demyelinate partially at midline, whereas C57BL/6 mice show robust demyelination, particularly at week 5.
“We found SJL mice demyelinate partially at midline (Figure 2A), whereas C57BL/6 mice show robust demyelination, particularly at week 5 2, 23, 35.”
From SJL Mice Exposed to Cuprizone Intoxication Reveal Strain and Gender Pattern Differences in Demyelination (2009) · cites this paper as [35]
IGF-1 has a highly protective role on oligodendrocytes.
“suggesting a highly protective role of IGF-1 on oligodendrocytes.”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2000b
In mice that constantly over-expressed IGF-1 within the brain, microgliosis was more pronounced after 3 weeks of cuprizone diet than in wild-type mice.
“microgliosis was more pronounced in mice that constantly over-expressed IGF-1 within the brain after 3 weeks of cuprizone diet (Mason et al., 2000b).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2000b
In IGF-1 over-expressing mice, mature oligodendrocytes were numerously present in the corpus callosum during demyelination instead of being nearly completely depleted.
“Furthermore, instead of being nearly completely depleted, mature oligodendrocytes were numerously present in the CC of IGF-1 over-expressing mice during demyelination”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2000b
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Metadata
- Authors
- Mason, J. L., Ye, P., Suzuki, K., D'Ercole, A. J., & Matsushima, G. K.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Pediatrics and Genetics (US)
- ORCID
- Suzuki, K.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2000-08-01
- Volume
- 20
- Issue
- 15
- Pages
- 5703-5708
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6772563
- OpenAlex
- W1536622417
- Cited by
- 237
- References
- 3
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 5 · 2019: 11 · 2018: 4 · 2017: 10 · 2016: 11 · 2015: 8 · 2014: 11 · 2013: 7 · 2012: 11
- FWCI
- 7.77
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Multiple Sclerosis Society
- Multiple Sclerosis Society
- National Institutes of Health (5r29ns035372-05)
- National Institute of Neurological Disorders and Stroke (NS 24453, R01NS024453, R01NS038891, NS-35372, NS38891)
- National Institute of Child Health and Human Development (HD03110)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD003110)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- insulin-like growth factor I, oligodendrocyte apoptosis, demyelination, remyelination, cuprizone, oligodendrocyte progenitors, corpus callosum, neuroprotection, transgenic mice, demyelinating disease
- MeSH terms
- Acute Disease, Animals, Brain Chemistry, Cell Survival, Chelating Agents, Corpus Callosum, Cuprizone, Demyelinating Diseases, Female, Insulin-Like Growth Factor I, Macrophages, Male, Mice, Inbred C57BL, Mice, Transgenic, Oligodendroglia, Stem Cells, Gene Expression, Apoptosis, Microglia, Recovery of Function, Mice
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