Fig 1: Association between SERPINA3 expression and survival time in glioblastoma tissues. SERPINA3, serpin peptidase inhibitor clade A member 3.
Fig 2: The upregulation of SERPINA3 in GSCs co-cultured with astrocytes. (A) Graphical representation of computational analysis using the datasets of GSCs and astrocyte co-cultured GSCs (GSE63037, GSE37120) and brain tumor-initiating cell response to microglia (GSE52127). (B) 10 overlapping genes were significantly upregulated compared with these 3 datasets, we identified SERPINA3 as candidate target for enhancing the invasion potential of GSCs. (C) Normalized expression of SERPINA3 in GSCs vs. astrocyte co-cultured GSCs or BTICs vs. BTICs exposed to MCM. GSCs, Glioblastoma stem-like cells; SERPINA3, serpin peptidase inhibitor clade A member 3; BTICs, brain tumor initiating cells; MCM, microglia conditioned medium.
Fig 3: Effect of SERPINA3-knockdown on matrix invasion by U251MG cells. (A) Photomicrographs of representative invasion cells. (B) Statistical analysis of cellular invasion of SERPINA3 knockdown cells. (**P<0.01 vs. NC). SERPINA3, serpin peptidase inhibitor clade A member 3. NC, negative control.
Fig 4: Overexpression of SERPINA3 in GBM compared to low-grade gliomas and non-tumor control. Representative hematoxylin and eosin staining micrograph and immunohistochemical staining of SERPINA3 in glioma tissues of various grades. All samples were scored using a previously described 12 point scale involving intensity and percentage of gliomas cells showing staining for SERPINA3 (see Materials and methods). (A) normal brain, (B) pilocytic astrocytomas, (C) diffuse astrocytomas, (D) anaplastic astrocytomas, and (E) glioblastomas multiforme. (F) Increased SERPINA3 expression correlates with progression of glioma. A marked increase in percentage of samples with high SERPINA3 expression was shown between glioblastomas multiforme and pilocytic astrocytomas (P=0.0484, ?2 test) and further between glioblastomas multiforme and anaplastic astrocytomas (P=0.0332, ?2 test). GBM, glioblastoma; SERPINA3, serpin peptidase inhibitor clade A member 3.
Fig 5: Characteristics of injury-induced disease-associated oligodendrocytes.a UMAP plot depicting the heterogeneous subsets of OPCs and oligodendrocytes in the intact and injured rhesus monkey spinal cord. A-OPC activated OPCs, H-OPC homeostatic OPC, D-OPC dividing OPC, MOL mature oligodendrocytes, MFOL myelin-forming oligodendrocytes, DOL disease-associated oligodendrocytes. b Gene expression visualized by UMAP plots. Each dot represents an individual cell colored according to the expression level. c Split UMAP plots showing the regional distribution of OPCs and oligodendrocyte subsets at different phases after SCI. d Dynamic changes in the proportion of subsets among OPCs or oligodendrocytes in different regions after SCI. e Violin plots showing the signature genes of DOL1 and DOL2 compared with other oligodendrocytes. f Immunostaining of SERPINA3 and APC in the lumbar spinal cord showing the different distribution of DOLs in CST and FG area at 7dpi. Scale bars, 500 µm on the left and 100 µm on the right. g Bar plot showing the proportion of SERPINA3 positive oligodendrocytes at different time points after SCI. Data are shown as mean ± SEM, n = 5 slices. ***p < 0.0001, two-sided Student’s t test. h Heatmap showing the expression of genes related to glycerolipid metabolic process and myelination in oligodendrocyte subsets. The color bar is scaled with the average expression of the corresponding genes. i Enriched GO terms of the upregulated genes in DOL1 from the SL compared with that from the SA area. P values (adjusted) were calculated using Benjamini–Hochberg false discovery rate (FDR). j Heatmap showing the expression of genes related to cellular stress in MOL1 from the SL. The color bar is scaled with the average expression of the corresponding genes. k Electron micrographs showing the autophagosome and autolysosome in the lumbar tissues at 6 months after SCI. Scale bars, 0.5 µm. Source data are provided as a Source Data file.
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