Regular ArticleNormal CNS Myelination in Transgenic Mice Overexpressing MHC Class I H-2Ld in Oligodendrocytes
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Cited by (26)
Crossing boundaries: Interplay between the immune system and oligodendrocyte lineage cells
2021, Seminars in Cell and Developmental BiologyCitation Excerpt :Similarly to IFNγ delivery to the developing CNS, overexpression of the MHC-I molecule H-2K in OLs (under the myelin basic protein promoter) also led to a hypomyelination phenotype, driven by a delay in developmental myelination and/or oligodendrocyte cell death [41,42]. Nevertheless, overexpression of another MHC-I molecule, H-2L under the proteolipid protein (Plp) promoter, did not present a disfunction in myelination [43]. Beta 2 microglobulin (B2m), which forms a complex with the heavy chain MHC-I molecule and the peptide antigen, is only weakly associated with H-2L, which could explain the differences in phenotype between these mice strains [43].
PERK activation preserves the viability and function of remyelinating oligodendrocytes in immune-mediated demyelinating diseases
2014, American Journal of PathologyCitation Excerpt :We have generated PLP/Fv2E-PERK transgenic mice that allow temporally controlled activation of PERK signaling specifically in oligodendrocytes in the absence of ER stress.11 These mice express Fv2E-PERK, an artificial PERK that is generated by fusing the eIF2α kinase effector domain of PERK to a polypeptide containing two modified FK506 binding domains (Fv2E),22 under the control of the mouse PLP transcriptional control region.23,24 We have demonstrated that PLP/Fv2E-PERK mice express the transgene product Fv2E-PERK specifically in oligodendrocytes and that the activity of Fv2E-PERK is tightly controlled by administration of the dimerizer AP20187.11
Functional recovery of callosal axons following demyelination: a critical window
2009, NeuroscienceCitation Excerpt :Cuprizone is a well described gliotoxic agent that alters the functions of OL mitochondria resulting in cell death. Eight wks old transgenic C57BL/6 female mice expressing enhanced green fluorescent proteins (EGFP) under the proteolipid protein (PLP) promoter (PLP_EGFP), (Fuss et al., 2001; Mallon et al., 2002) were fed with 0.2% cuprizone diet for 1.5 to 6 wks (demyelination group, DM: 1.5 wkDM, 3 wkDM, and 6 wkDM), resulting in demyelination of the CC. The decrease in myelin was assessed by myelin oligodendrocyte glycoprotein (MOG) immunolabelling intensity in the delineated CC.
Assaying the functional effects of demyelination and remyelination: Revisiting field potential recordings
2009, Journal of Neuroscience MethodsChapter 1 Genetic Dissection of Neural Circuits and Behavior in Mus musculus
2009, Advances in GeneticsCitation Excerpt :For example, the use of promoters like Nestin (Cheng et al., 2004), PrP (Fischer et al., 1996), and neuron‐specific enolase (Forss‐Petter et al., 1990) result in transgene expression throughout the brain but not in other parts of the body. For further restriction to specific brain regions or cell types, researchers used more specific promoters, including the α‐CaMKII promoter for postnatal forebrain specific expression in excitatory neurons (Abel et al., 1997; Mayford et al., 1996), glial fibrillary acidic protein (GFAP) for astrocyte‐specific expression (Brenner et al., 1994; Casper et al., 2007; Halassa et al., 2009; Pascual et al., 2005), proteolipid protein (PLP) oligodendrocyte‐specific expression (Fuss et al., 2001), and L7 for expression in cerebellar Purkinje cells and retinal bipolar neurons (Oberdick et al., 1990). Large‐scale screening projects have been initiated to determine the brain expression patterns of a tremendous number of specific promoters, allowing researchers to choose a promoter that targets a particular class of neurons, such as those that produce a specific neurotransmitter, or express a specific receptor.
Down-regulation of polysialic acid is required for efficient myelin formation
2007, Journal of Biological ChemistryCitation Excerpt :Generation of PLP-PST Transgenic Mice−Mouse ST8SiaIV was amplified by PCR using oligonucleotides PSTsense (5′-GCAAGCTTCCATGCGCTCAATTAGAAAACG-3′) and PSTanti (5′-GCTCTAGATTATTGCTTCATGCACTTTCC-3′), digested with HindIII and XbaI (introduced restriction sites are underlined in the primer sequences), treated with Klenow enzyme (fill-in reaction), and ligated into the PmeI site of the PLP promoter cassette (19) (kindly provided by W. B. Macklin (Cleveland Clinic Foundation)) (see Fig. 1A).
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