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Glio

Real pictures of the glio delivered by gather.site, each with its paper.

7 pictures and 7 papers.

Gallery

Biological performance of bioprinted GelMA/dECM composite constructs for in vitro GBM modeling. (A) Live/Dead images at day 1 demonstrating uniformly high cell viability across printed constructs and DAPI/F-actin (green)/vimentin (red) staining at day 7 showing enhanced cytoskeletal organization and increased vimentin expression in dECM-containing groups, most prominently in C-dECM (C-CB) constructs. (B) Quantified cell viability (n = 3) after printing (>93-95% survival). (C) Quantification of vimentin+ area (n = 3). (D,E) Gene expression analysis of glioma stem-like markers (CD44, CD133) and oncogenic growth factor signaling components (EGFR, HGF) in control, NC-CB, and C-CB constructs (n = 3). (F) Heat map of GBM-associated genes (e.g., TGF-beta, IL-6, PDGF-beta, CCN2, CXCL12) (n = 3). (G) Representative RT-qPCR electrophoresis. (H) Schematic of growth factor-mediated PI3K-AKT/MAPK/STAT3 pathways associated with stemness, invasion, and stromal remodeling. (I) Schematic and representative images of the 3D invasion assay consisting of adjacent cellular and acellular regions. Live/Dead staining on day 1 and DAPI (blue)/F-actin (red) staining on day 7. White arrows indicating the direction of cell invasion. (J) Experimental timeline of the temozolomide (TMZ) response assay. (K) Live/Dead images before TMZ treatment on day 7 and after 72 h of TMZ treatment on day 10. (L) Time-dependent changes in cell proliferation of the control, NC-CB, and C-CB constructs at 0, 24, 48, and 72 h after TMZ treatment (n = 3), measured by CCK assay. (M) Schematic illustrating TMZ-induced DNA damage, p53-associated stress responses, and major drug-resistance mechanisms. (N) Relative expression of the drug resistance-associated genes (ABCG2 and MGMT), the DNA damage response-associated gene (p53), the chemokine signaling-associated gene CXCL12, and the oncogenic signaling-associated gene EGFR after 72 h of TMZ treatment (n = 3). One-way ANOVA followed by Tukey's HSD post-hoc test was used for multiple comparisons. (Figure 6.)

An, Jo, Kim et al 2026, Theranostics · CC BY 4.0

Nlgn1-3 are efficiently and selectively deleted in astrocytes by crossing triple Nlgn1-3 conditional KO mice with Aldh1l1-CreER T2 driver mice and inducing Cre-activity with tamoxifen early during postnatal development. ( A ) Breeding strategy. Triple conditional KO mice carrying floxed Nlgn1, Nlgn2, and Nlgn3 alleles or mice with a Cre-sensitive tdTomato (tdT) reporter allele (Ai14) were crossed with pan-astrocyte, tamoxifen-inducible Aldh1l1-CreER T2 BAC transgenic mice. ( B, C ) Two different tamoxifen-induced Cre-activation schedules were used to delete Nlgn1-3 in astrocytes. Aldh1l1-CreER T2 mice and controls (littermate Nlgn1-3 cKO mice lacking the Aldh1l1-CreER T2 allele) were injected with tamoxifen at P10 and P11 ( B ) or at P1 ( C ). ( D, E ) To confirm the specificity and efficiency of the deletion of target genes in astrocytes using the Aldh1l1-CreER T2 BAC transgenic mouse line via tamoxifen injection at P1, Cre-recombination was visualized in the hippocampus ( D ) and primary visual cortex ( E ) via expression of tdT in reporter mice (magenta). Sections were additionally labeled for NeuN to mark neurons (green) and S100beta to mark astrocytes (blue). ( F ) The Aldh1l1-CreER T2-induced deletion of floxed genes produced by P1 tamoxifen injections is effective and selective for astrocytes as quantified using expression of tdTomato in reporter mice. tdTomato expression was quantified in the CA1 region of the hippocampus (the S. oriens, S. pyramidale, S. radiatum, and S. lacunosum-moleculare), the dentate gyrus (molecular layer [ML], granule cell layer [GCL], and hilus), and layer IV of the primary visual cortex. (mouse (Aldh1l1-CreER T2 x Ai14 tdTomato reporter mice; P1 tamoxifen injection showing pan-astrocyte Cre activity in hippocampus and visual cortex); Figure 2..)

Golf, Trotter, Wang et al 2026, eLife · CC BY 4.0

Histological characterization of PDTC and PDNS. (A) Representative hematoxylin and eosin (H&E) staining of GBM PDTCs cultured under different media conditions to evaluate preservation of tissue morphology and architecture (scale bar = 50 um). Organotypic hippocampal slice culture medium and serum-free NeuroCult medium maintained tissue integrity most effectively, whereas other serum-free media resulted in progressive loss of structural organization. (B) Representative images illustrating morphological differences between PDTCs and matched PDNS generated from two independent patient specimens (upper and lower rows, respectively, NeuroCult media). PDTCs preserved native tissue architecture and cellular heterogeneity, whereas PDNS formed compact multicellular spheroids with reduced structural complexity (scale bar = 100 um). (C) Quantification of stem cell markers in native tumor tissue, PDTCs, and PDNS (n = 4 patients, NeuroCult media). Expression of stem cell-associated markers (Survivin, Olig2, SOX2, Nestin, and CD44) was compared between native tissue, PDTCs, and PDNS. (D) CD44 expression differed significantly between native tissue and PDNS, although substantial inter-patient heterogeneity was observed. (E) GFAP expression was preserved across culture conditions, whereas CD31-positive endothelial cells were largely absent in PDNS. Representative immunohistochemical staining for HIF1alpha is shown in PDTC. Statistical analysis was performed using the Kruskal-Wallis test followed by Dunn's multiple-comparison test (*p < 0.05, **p < 0.01, ****p < 0.0001). (Fig. 2.)

Kohler, Hess, Koloske et al 2026, Journal of Neuro-Oncology · CC BY 4.0

Effects of chronic restraint stress (CRS) on glial fibrillary acidic protein (GFAP) integrated density in different stress- and pain-related brain regions of male and female wild-type (WT) and CX3CR1 knock-out (KO) mice; in the periaqueductal gray matter (PAG) (A, B) and hippocampus Cornu Ammonis 3 (CA3) (C, D). Data are presented as mean +/- SEM, animals with individual plots (n=6/group). Two-way analysis of variance (ANOVA), followed by Tukey's tests; *p<0.05, **p<0.001, ***p<0.0001 vs. indicated groups. Representative images show the GFAP+ astrocyte cells in PAG in male mice (E) Representative images of astrocyte-microglia interactions of the PAG in control and stressed WT male animals. Confocal images show microglia- and (green) astrocyte processes (red) contacting in the PAG of control (F) and after CRS (G) WT animals. (Figure 4.)

Fulop, Kiraly, Petrak et al 2026, Frontiers in Immunology · CC BY 4.0

Elevated expression of PTPRZ1 at the invasive tumor margin across human glioma grades. (A) Representative images of immunohistochemical (IHC) staining for PTPRZ1 within matched spatially distinct regions from five glioma patients. (B) T1-weighted MRI approximate surgical sampling locations corresponding to the spatial regions in (A): intratumoral core (blue), peritumoral region (green), and invasive tumor margin (orange). (C) PTPRZ1 expression within individual patients. Line graph showing the PTPRZ1 IHC Score for each tissue section across the Intratumor, Peritumor, and Tumor margin regions for all five patients (P1-P5). (D) Collective quantitative analysis of PTPRZ1 expression in gliomas. Dot plot summarizing the IHC Scores for the three spatial regions across all analyzed tumor tissues (RM-ANOVA test, * P < 0.05, **P < 0.01). (Fig. 5.)

Yi, Qin, Guo et al 2026, Journal of Translational Medicine · CC BY 4.0

Host TLR4 deficiency reduces glioma expansion and invasion in organotypic brain slices. (A) Representative confocal scans and 3D reconstructions of organotypic brain slices (OBS) labeled with mCherry GL261 glioma cells from WT (n = 7) and TLR4-KO (n = 6) mice. OBS were obtained from 14-16-day-old C57BL/6 mice and inoculated with 5,000 GL261-mCherry cells. Scans were performed with a Leica SPE confocal microscope using a 10x magnification 5 days after injection. Scale bars: 500 um. (B) Quantification of tumor volume (top) and tumor surface infiltration area (bottom) from 3D reconstructions of mCherry fluorescence signal. Both tumor volume and infiltration area were significantly reduced in TLR4-KO slices compared with WT controls. (Figure 2.)

Haneke, Efe, Dzaye et al 2026, Frontiers in Oncology · CC BY 4.0

VCAM1 is expressed in a subset of GLAST+ astrocytes in glioma-bearing mice. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::Ai14 mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week resting period. On day 1, 5,000-6,000 eGFP+ 73C or GL261-luc glioma cells were implanted beneath the hippocampus. Tumor-bearing mice were harvested on day 10 (eGFP+ 73C) or day 20 (GL261-luc). (B) Immunofluorescence staining of VCAM1 in eGFP+ 73C gliomas at day 10 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (B) 1 mm; (a), 500 um; (a', b'), 100 um. (C) Immunofluorescence staining of VCAM1 in GL261-luc gliomas at day 20 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (C) 1 mm; (a), 500 um; (a'), 100 um. (Figure 3.)

Dai, Zheng, Luo et al 2026, Frontiers in Oncology · CC BY 4.0

Papers

  1. Haneke H, Efe IE, Dzaye O, Kettenmann H, Yalcin F. Host TLR4 activation by tenascin-C is associated with MMP14-dependent glioma invasion. Front Oncol. 2026;16:1915071. PMID: 42774130.
  2. Köhler F, Hess K, Koloske C, Gaunitz F, Rosahl SK, Gerlach R, et al. Patient-derived tissue cultures complement neurospheres for preclinical evaluation of AAV-mediated gene delivery in glioblastoma. J Neurooncol. 2026;179:93. PMID: 42771216.
  3. Yi L, Qin S, Guo M, Wang X, Zhang Y, Guo P, et al. Spatial enrichment of PTPRZ1 in the peritumoral niche drives glioblastoma migration via the OPA1/ROS/CDH2 axis. J Transl Med. 2026;24:1103. PMID: 42661193.
  4. An S, Jo S, Kim G. A mechanobiology-driven cell-derived ECM bioink for engineering 3D glioblastoma tumor microenvironment models. Theranostics. 2026;16:8361-8384. PMID: 42559402.
  5. Golf SR, Trotter JH, Wang J, Nakahara G, Han X, Wernig M, et al. Deletion of neuroligins from astrocytes does not detectably alter synapse numbers or astrocyte cytoarchitecture by maturity. Elife. 2026;12:RP87589. PMID: 42549988.
  6. Fülöp B, Király , Petrák R, Müller J, Biró-Sütő T, Kormos V, et al. Microglial CX3CR1 signaling mediates stress-induced pain behavior in mice. Front Immunol. 2026;17:1869876. PMID: 42459679.
  7. Dai J, Zheng H, Luo J, Dai M, Hu XL, Sun W. Glia-derived VCAM1 promotes glioma progression. Front Oncol. 2026;16:1802953. PMID: 42109665.

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