Pairwise comparisons for genotype within region*length*genotype interaction in the SVZ. (JPG 288 kb

Francis Szele (3501209)

James Hillis (3501212)

Julie Davies (3501206)

Mayara Mundim (3501215)

Osama Al-Dalahmah (3501203)

Journal of Neuroinflammation

PubMed

Cuprizone causes loss of MBP expression in the olfactory bulb. A and B: OB sections with MBP immunohistochemistry from WT mice. Dotted box shows region of images in B. GL: glomerular layer, EPL: external plexiform layer, MCL/IPL: mitral cell layer/internal plexiform layer, GrL: granular layer. Scale bars 500 mm (A) and 100 mm (B). C: Graphs showing percentage of pixels with fluorescence intensity above threshold in the glomerular, external plexiform, and granular layers. Statistics calculated as repeated-measures ANOVA with N = 6. Graphs show mean ± SEM. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. (TIF 18577 kb

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Additional file 6: Figure S3. of Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

Ki67 and Mash1 immunohistochemistry in the SVZ. Representative examples of Ki67 and Mash1 immunohistochemistry in the SVZ. Scale bar 50 Îźm. (TIF 5734 kb

Additional file 3: Figure S2. of Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

Additional file 4: Table S2. of Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

Gal-3 absence does not alter candidate gene expression. A: Graph shows the relative expression of the candidate genes Ccl2, Ccr2, Egfr, and Mmp9 in the SVZ of Gal-3 +/+ and Gal-3 −/− mice. It demonstrates fold change compared to Gal-3 +/+ mice for quantities normalized to the housekeeping gene B2m. Graph shows mean ± SEM. Graph demonstrates fold change compared to Gal-3 +/+ mice. Statistics calculated as t test using SPSS. No significant differences found. B: Gal-3 absence is not compensated by other galectins. Graph shows qPCR comparison of SVZ galectin expression in Gal-3 +/+ and Gal-3 −/− mice. It demonstrates fold change compared to Gal-3 +/+ mice for quantities normalized to the housekeeping gene B2m. Genes include Lgals1, 3, 8, and 9, which correspond to Gal-1, 3, 8, and 9, respectively. Statistics calculated as t test with N = 3 samples per genotype, each sample containing pooled SVZs from four mice. Graph shows mean ± SEM. ***p < 0.001. (TIF 9099 kb

Additional file 1: Figure S1. of Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

James M. Hillis

Julie Davies

Mayara Vieira Mundim

Osama Al-Dalahmah

Francis G. Szele

Crossref

Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

BackgroundCuprizone leads to demyelination of the corpus callosum (CC) and activates progenitor cells in the adjacent subventricular zone (SVZ), a stem cell niche which contributes to remyelination. The healthy SVZ contains semi-activated microglia and constitutively expresses the pro-inflammatory molecule galectin-3 (Gal-3) suggesting the niche uniquely regulates inflammation. MethodsWe studied the inflammatory response to cuprizone in the SVZ and CC in Gal-3 knockout mice using immunohistochemistry and with the in vitro neurosphere assay. ResultsCuprizone caused loss of myelin basic protein (MBP) immunofluorescence in the CC suggesting demyelination. Cuprizone increased the density of CD45+/Iba1+ microglial cells and also increased Gal-3 expression in the CC. Surprisingly, the number of Gal-3+ and CD45+ cells decreased in the SVZ after cuprizone, suggesting inflammation was selectively reduced therein. Inflammation can regulate SVZ proliferation and indeed the number of phosphohistone H3+ (PHi3+) cells decreased in the SVZ but increased in the CC in both genotypes after cuprizone treatment. BrdU+ SVZ cell numbers also decreased in the SVZ after cuprizone, and this effect was significantly greater at 3 weeks in Gal-3 −/− mice compared to WT, suggesting Gal-3 normally limits SVZ cell emigration following cuprizone treatment. ConclusionsThis study reveals a uniquely regulated inflammatory response in the SVZ and shows that Gal-3 participates in remyelination in the cuprizone model. This contrasts with more severe models of demyelination which induce SVZ inflammation and suggests the extent of demyelination affects the SVZ neurogenic response

Hillis, James M

Davies, Julie

Mundim, Mayara Vieira

Al-Dalahmah, Osama

Szele, Francis

Oxford University Research Archive

English

Cuprizone demyelination induces a unique inflammatory response in the subventricular zone.

PHi3+ cells int he SVZ and CC after cuprizone treatment. (JPG 380 kb

Additional file 2: Table S1. of Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

http://repositorio.unifesp.br/handle/11600/51163

Additional file 4: Table S2. of Cuprizone demyelination induces a unique inflammatory response in the subventricular zone

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