Function of B-Cell CLL/Lymphoma 11B in Glial Progenitor Proliferation and Oligodendrocyte Maturation

Wang, Chih Yen; Sun, Yuan; Fang, Kuan; Ho, Chia Hsin; Yang, Chu-Sing; Tzeng, Shun Fen

doi:10.3389/fnmol.2018.00004

Cited by 16 publications

(9 citation statements)

References 44 publications

(64 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specifically, we found BCL11B (CTIP2), a negative regulator of glial progenitor cell differentiation to be significantly increased at the glial scar (Fig. 8d , left) 53 . Conversely, we found RXRG, a positive regulator of OPC differentiation, and remyelination, to be significantly depleted (Fig.…”

Section: Resultsmentioning

confidence: 83%

Spatially mapped single-cell chromatin accessibility

et al. 2021

View full text Add to dashboard Cite

High-throughput single-cell epigenomic assays can resolve cell type heterogeneity in complex tissues, however, spatial orientation is lost. Here, we present single-cell combinatorial indexing on Microbiopsies Assigned to Positions for the Assay for Transposase Accessible Chromatin, or sciMAP-ATAC, as a method for highly scalable, spatially resolved, single-cell profiling of chromatin states. sciMAP-ATAC produces data of equivalent quality to non-spatial sci-ATAC and retains the positional information of each cell within a 214 micron cubic region, with up to hundreds of tracked positions in a single experiment. We apply sciMAP-ATAC to assess cortical lamination in the adult mouse primary somatosensory cortex and in the human primary visual cortex, where we produce spatial trajectories and integrate our data with non-spatial single-nucleus RNA and other chromatin accessibility single-cell datasets. Finally, we characterize the spatially progressive nature of cerebral ischemic infarction in the mouse brain using a model of transient middle cerebral artery occlusion.

show abstract

Section: Resultsmentioning

confidence: 83%

Spatially mapped single-cell chromatin accessibility

et al. 2021

View full text Add to dashboard Cite

show abstract

“…OPCs that were generated from neural stem cells derived from the brain tissues of mouse embryos at 14.5 days were plated onto poly- d -lysine (PDL; Sigma; Cat# P0899) -coated dishes and maintained in the growth medium consisting of DMEM/F12 medium (Thermo Fisher, Cat# 12400024), 2% B27 supplement (Thermo Fisher; Cat# 17504044), 1% N2 supplement (Thermo Fisher; Cat# 17502048), 10 ng/ml epidermal growth factor (ProSpec; Cat# GFH-26-100), 10 ng/ml fibroblast growth factor-2 (Cell Guidance Systems; Cat# PPH146), and 10 ng/ml platelet-derived growth factor-AA (ProSpec; Cat# CYT-341). To induce the differentiation of OPCs into mature OLGs with expression of myelin proteins [31], OPCs were cultured for 7 days in OLG differentiation medium (DM) containing DMEM medium (Thermo Fisher; Cat# 12100-046), 1% Penicillin–Streptomycin (Thermo Fisher; Cat#15140-122), 1 mM sodium pyruvate (Sigma; Cat# P2256), 0.1% bovine serum albumin (Sigma; Cat# A7030), 50 μg/ml apotransferrin (Sigma; Cat# T2252), 5 μg/ml insulin (Sigma; Cat# I6634), 30 nM sodium selenite (Sigma; Cat# S5261), 10 nM biotin (Sigma; Cat# B4639), 10 nM hydrocortisone (Sigma; Cat# H0888), 15 nM triiodothyronine (Sigma; Cat# T6397), 10 ng/ml ciliary neurotrophic factor (ProSpec; Cat# CYT-272), and 5 μg/ml N-acetyl-cysteine (Sigma; Cat# A9165). To determine the effect of IL-33 on OLG maturation, OLGs after a 6-day incubation in DM were continuously treated with mouse recombinant IL-33 (CellGS, Cat# GFM36) in DM for 24 h.…”

Section: Methodsmentioning

confidence: 99%

Chronic exposure to high fat diet triggers myelin disruption and interleukin-33 upregulation in hypothalamus

Huang

Tsai

et al. 2019

BMC Neurosci

Self Cite

View full text Add to dashboard Cite

Background Hypothalamic inflammation including astrogliosis and microglia activation occurs after intake of high fat diet (HFD) in rodent models or in obese individuals. However, the effect of chronic HFD feeding on oligodendrocytes (OLGs), a myelin-producing glial population in the central nervous system (CNS), remains unclear. In this study, we used 8-week old male C57BL/6 mice fed by HFD for 3–6 months to induce chronic obesity. Results The transmission electron microscopy imaging analysis showed that the integrity of hypothalamic myelin was disrupted after HFD feeding for 4 and 6 months. Moreover, the accumulation of Iba1 + -microglia with an amoeboid hypertrophic form was continually observed in arcuate nucleus of HFD-fed mice during the entire feeding time period. Interleukin-33 (IL-33), a tissue alarmin upon injury to the CNS, was detected with an increased level in hypothalamus after HFD feeding for 3 and 4 months. Furthermore, the in vitro study indicated that exposure of mature OLGs to IL-33 impaired OLG cell structure along with a decline in the expression of myelin basic protein. Conclusions Altogether, our findings demonstrate that chronic HFD feeding triggers hypothalamic myelin disruption in accompany with IL-33 upregulation and prolonged microglial activation in hypothalamus. Given that the addition of exogenous IL-33 was harmful for the maturation of OLGs, an increase in IL-33 by chronic HFD feeding might contribute to the induction of hypothalamic myelin disruption. Electronic supplementary material The online version of this article (10.1186/s12868-019-0516-6) contains supplementary material, which is available to authorized users.

show abstract

“…In oligodendrocytes, 56 TF motifs were significantly different between the stroke and contralateral hemisphere, many of which (78.6%) corresponded to higher enrichment in stroke as compared to contralateral. Specifically, we found BCL11B (CTIP2), a negative regulator of glial progenitor cell differentiation to be significantly increased at the glial scar around the infarct (Figure 4i, left) 51 .…”

Section: Scimap-atac In Cerebral Ischemia Reveals Spatially Progressimentioning

confidence: 91%

Spatially mapped single-cell chromatin accessibility

Thornton

Mulqueen

Torkenczy

et al. 2019

Preprint

View full text Add to dashboard Cite

High-throughput single-cell genomic assays resolve the heterogeneity of cell states in complex tissues, however, the spatial orientation within the network of interconnected cells is lost. As cell localization is a necessary dimension in understanding complex tissues and disease states, we present a novel method for highly-scalable spatially-resolved single-cell profiling of chromatin states. We use high density multiregional sampling to perform single-cell combinatorial indexing on Microbiopsies Assigned to Positions for the Assay for Transposase Accessible Chromatin (sciMAP-ATAC) to produce single-cell data of equivalent quality to non-spatial single-cell ATAC-seq. We apply sciMAP-ATAC in the adult mouse cortex to discriminate cortical layering of glutamatergic neurons and establish the spatial ordering of single cells within intact tissue. We then leverage this spatiallyoriented cell dataset by combining it with non-spatially resolved whole brain sci-ATAC-seq data and assess layer-specific marker gene chromatin accessibility and transcription factor motif enrichment. Using sciMAP-ATAC seq, we identify sets of regulatory elements that spatially vary in the cortex, which includes canonical layer-specific markers and previously unannotated putative regulatory elements.

show abstract

Function of B-Cell CLL/Lymphoma 11B in Glial Progenitor Proliferation and Oligodendrocyte Maturation

Cited by 16 publications

References 44 publications

Spatially mapped single-cell chromatin accessibility

Spatially mapped single-cell chromatin accessibility

Chronic exposure to high fat diet triggers myelin disruption and interleukin-33 upregulation in hypothalamus

Spatially mapped single-cell chromatin accessibility

Contact Info

Product

Resources

About