Protein kinase C activity modulates myelin gene expression in enriched oligodendrocytes - PubMed (original) (raw)
. 1993 Apr 1;34(5):571-88.
doi: 10.1002/jnr.490340509.
Affiliations
- PMID: 7683060
- DOI: 10.1002/jnr.490340509
Protein kinase C activity modulates myelin gene expression in enriched oligodendrocytes
K Asotra et al. J Neurosci Res. 1993.
Abstract
Protein kinase C (PKC) and its potential role in myelin gene expression were investigated in primary cultured rat oligodendrocytes. The major myelin genes were expressed in a developmentally coordinated manner in cultured oligodendrocytes. PKC activity in these cells was similarly regulated with differential expression of PKC isozyme mRNAs. PKC-gamma mRNA was expressed transiently and was most abundant in 9-day cells in vitro. PKC-alpha and PKC-beta mRNAs were present at low levels throughout development in these cells, and their expression increased in 18-25 day cells. Immunocytochemical colocalization of PKC with oligodendrocyte-specific markers--O4, galactosyl cerebroside, MBP, and PLP--in enriched oligodendrocyte cultures suggested that the PKC enzyme activities assayed in these cultures were predominantly contributed by oligodendrocytes. PKC inhibition resulting from long-term exposure to 4 beta-phorbol-12,13-dibutyrate (4 beta-PDB) reduced steady-state levels of MBP, PLP, MAG, CNP, and PKC-alpha mRNAs, as detected by slot blots or in situ hybridization, and downregulated the oligodendrocyte-specific markers O4, galactosyl cerebroside, and the major constituent proteins MBP and PLP, as detected by immunocytochemistry. PKC-mediated downmodulation of myelin gene expression was most profound in normally differentiating oligodendrocytes at or before the onset of myelin protein synthesis. Six-day oligodendrocytes were most susceptible to such modulation. To elucidate the mechanism of reduction in various myelin gene messages upon modulation of PKC, we analyzed mRNA levels in oligodendrocytes, which were pretreated with either the transcriptional inhibitor actinomycin D or the protein synthesis blocker cycloheximide before exposure to 4 beta-PDB. Our results demonstrate that the PKC inhibition-mediated loss in myelin mRNA levels did not require the transcription of any genes, but appeared to be at least partially dependent on continuous protein synthesis.
Similar articles
- Developmental expression of protein kinase C isozymes in oligodendrocytes and their differential modulation by 4 beta-phorbol-12,13-dibutyrate.
Asotra K, Macklin WB. Asotra K, et al. J Neurosci Res. 1994 Oct 15;39(3):273-89. doi: 10.1002/jnr.490390305. J Neurosci Res. 1994. PMID: 7869420 - Protein kinase C inhibitors counteract the ethanol effects on myelin basic protein expression in differentiating CG-4 oligodendrocytes.
Bichenkov E, Ellingson JS. Bichenkov E, et al. Brain Res Dev Brain Res. 2002 Nov 15;139(1):29-38. doi: 10.1016/s0165-3806(02)00512-6. Brain Res Dev Brain Res. 2002. PMID: 12414091 - Protein kinase C in cultured adult human oligodendrocytes: a potential role for isoform alpha as a mediator of process outgrowth.
Yong VW, Dooley NP, Noble PG. Yong VW, et al. J Neurosci Res. 1994 Sep 1;39(1):83-96. doi: 10.1002/jnr.490390111. J Neurosci Res. 1994. PMID: 7807594 - The distribution of myelin basic protein mRNAs within myelinating oligodendrocytes.
Brophy PJ, Boccaccio GL, Colman DR. Brophy PJ, et al. Trends Neurosci. 1993 Dec;16(12):515-21. doi: 10.1016/0166-2236(93)90196-s. Trends Neurosci. 1993. PMID: 7509522 Review. - Developmental regulation of myelin-associated genes in the normal and the myelin deficient mutant rat.
Gordon MN, Kumar S, Espinosa de los Monteros A, Scully S, Zhang MS, Huber J, Cole RA, de Vellis J. Gordon MN, et al. Adv Exp Med Biol. 1990;265:11-22. doi: 10.1007/978-1-4757-5876-4_2. Adv Exp Med Biol. 1990. PMID: 1696059 Review.
Cited by
- Huntington disease oligodendrocyte maturation deficits revealed by single-nucleus RNAseq are rescued by thiamine-biotin supplementation.
Lim RG, Al-Dalahmah O, Wu J, Gold MP, Reidling JC, Tang G, Adam M, Dansu DK, Park HJ, Casaccia P, Miramontes R, Reyes-Ortiz AM, Lau A, Hickman RA, Khan F, Paryani F, Tang A, Ofori K, Miyoshi E, Michael N, McClure N, Flowers XE, Vonsattel JP, Davidson S, Menon V, Swarup V, Fraenkel E, Goldman JE, Thompson LM. Lim RG, et al. Nat Commun. 2022 Dec 21;13(1):7791. doi: 10.1038/s41467-022-35388-x. Nat Commun. 2022. PMID: 36543778 Free PMC article. - Neuron-specific ablation of the Krabbe disease gene galactosylceramidase in mice results in neurodegeneration.
Kreher C, Favret J, Weinstock NI, Maulik M, Hong X, Gelb MH, Wrabetz L, Feltri ML, Shin D. Kreher C, et al. PLoS Biol. 2022 Jul 5;20(7):e3001661. doi: 10.1371/journal.pbio.3001661. eCollection 2022 Jul. PLoS Biol. 2022. PMID: 35789331 Free PMC article. - Neuroimmune mechanisms in Krabbe's disease.
Potter GB, Petryniak MA. Potter GB, et al. J Neurosci Res. 2016 Nov;94(11):1341-8. doi: 10.1002/jnr.23804. J Neurosci Res. 2016. PMID: 27638616 Free PMC article. Review. - Systematic Review of Pharmacological Properties of the Oligodendrocyte Lineage.
Marinelli C, Bertalot T, Zusso M, Skaper SD, Giusti P. Marinelli C, et al. Front Cell Neurosci. 2016 Feb 12;10:27. doi: 10.3389/fncel.2016.00027. eCollection 2016. Front Cell Neurosci. 2016. PMID: 26903812 Free PMC article. Review. - Genetic markers of white matter integrity in schizophrenia revealed by parallel ICA.
Gupta CN, Chen J, Liu J, Damaraju E, Wright C, Perrone-Bizzozero NI, Pearlson G, Luo L, Michael AM, Turner JA, Calhoun VD. Gupta CN, et al. Front Hum Neurosci. 2015 Mar 3;9:100. doi: 10.3389/fnhum.2015.00100. eCollection 2015. Front Hum Neurosci. 2015. PMID: 25784871 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous