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dapi  (SouthernBiotech)
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SouthernBiotech dapi
ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
Dapi, supplied by SouthernBiotech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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dapi fluoromount g  (SouthernBiotech)
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ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
Dapi Fluoromount G, supplied by SouthernBiotech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antifluorescence quencher  (SouthernBiotech)
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SouthernBiotech antifluorescence quencher
ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
Antifluorescence Quencher, supplied by SouthernBiotech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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dapi medium  (SouthernBiotech)
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ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
Dapi Medium, supplied by SouthernBiotech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fluoromount g with dapi  (SouthernBiotech)
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ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
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4 6 diamidino 2 202 phenylindole  (SouthernBiotech)
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ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
4 6 Diamidino 2 202 Phenylindole, supplied by SouthernBiotech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were <t>counterstained</t> with <t>DAPI</t> (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.
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ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were counterstained with DAPI (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.

Journal: Advanced Science

Article Title: Astrocyte‐Associated ABCA1/APOE Responses Accompany Hippocampal Lipid Remodeling and Ectopic Neuronal Accumulation During Epileptogenesis

doi: 10.1002/advs.78329

Figure Lengend Snippet: ABCA1 and APOE expression is altered in hippocampal astrocytes in KA‐ and pilocarpine‐induced epilepsy models. (A,B) Western blot analysis (A) and quantification of APOE/β‐Tubulin (B) in the mouse hippocampus at 1, 2, 4, and 8 weeks after KA‐induced status epilepticus (SE) ( n = 5 per group). (C,D) Quantification of the percentage of APOE‐expressing astrocytes (APOE + /GFAP + double‐positive, C) and ABCA1/APOE‐co‐expressing astrocytes (ABCA1 + /APOE + /GFAP + triple‐positive, D) relative to total GFAP + cells in the hippocampal hilus at 1 week after KA‐induced SE ( n = 5 per group). (E) Representative immunofluorescence images showing the expression of APOE (red), ABCA1 (green), and GFAP (astrocyte marker, cyan) in the hippocampus at 1 week after KA‐induced SE. Nuclei were counterstained with DAPI (blue). White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). (F–H) Western blot analysis of ABCA1 and APOE expression in the pilocarpine‐induced epilepsy model (F), with quantification of relative ABCA1/GAPDH (G) and APOE/β‐Tubulin (H) protein levels at different time points ( n = 3 per group). (I) Representative multiplex immunofluorescence images showing expression of APOE (red), ABCA1 (green), GFAP (cyan) and DAPI (blue) at 1 week after pilocarpine‐induced SE. White dashed boxes indicate the regions shown in the magnified insets, and white arrowheads indicate APOE and ABCA1 immunoreactivity associated with GFAP + astrocytic profiles. Scale bars: 20 µm (main panels) and 8 µm (magnified insets). Data are presented as mean ± SD. Western blot data were analyzed using two‐way ANOVA followed by Sidak's multiple‐comparisons test. Immunofluorescence data were analyzed using two‐sided unpaired Welch's t‐tests. * p < 0.05, ** p < 0.01, **** p < 0.0001. Numbers above bars indicate exact non‐significant P values.

Article Snippet: Cell nuclei were subsequently counterstained with DAPI (SBA‐0100‐20, 1:1000, SouthernBiotech).

Techniques: Expressing, Western Blot, Analysis, Immunofluorescence, Marker, Multiplex Assay