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Huabio Inc neuron marker tuj 1
Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining <t>against</t> <t>Tuj-1</t> and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.
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Images

1) Product Images from "A cell motility-based selective hydrogel enables rapid generation of nerve-repairing blood clots"

Article Title: A cell motility-based selective hydrogel enables rapid generation of nerve-repairing blood clots

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.05.015

Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.
Figure Legend Snippet: Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.

Techniques Used: Derivative Assay, Membrane, Staining, CCK-8 Assay, Immunostaining, Control, Migration



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Huabio Inc neuron marker tuj 1
Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining <t>against</t> <t>Tuj-1</t> and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.
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FGFR-agonist regulates cellular behaviors of NPCs. ( A ) The proliferation of NPCs was evaluated at 24-hour and 72-hour time points following treatments with bFGF or FGFR-agonist, using a CCK8 kit. ( B ) Serum-starved NPCs were placed in the upper chamber, while bFGF(20 ng/mL) and FGFR-agonist (40 nM) were included in the lower chamber for 24 h and stained, followed visualization under light microscopy. Scale bar = 100 μm. ( C ) The data from the Transwell assay are quantified to assess the impact of different treatments on NPC migration. Data are presented as mean ± SD (n = 6). ( D ) Representative images showing the undifferentiated NPCs (Nestin-positive) and differentiated neurons <t>(Tuj-1</t> positive) NPCs treated with bFGF, FGFR-agonist and Ctrl-oligo for 7 days and subjected to immunofluorescence staining. Scale bar = 100 μm. ( E ) The ratios of Nestin-positive cells and Tuj-1-positive cells are quantified against total cells (DAPI-positive). Data are presented as mean ± SD (n = 3), with **p < 0.001, as determined by unpaired t-tests. ( F ) Representative images of neurospheres generated by NPCs cultured in suspension for 10 days in the presence or absence of bFGF (20 ng/mL), FGFR-agonist (40 nM), or FGFR-agonist (200 nM). The scale bar = 100 μm. (G) Quantification of the changes in neurosphere volume over a 10-day culture period under various treatment conditions. Data are displayed as mean ± SD (n = 3), with **p < 0.0001, as determined by one-way ANOVA
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FGFR-agonist regulates cellular behaviors of NPCs. ( A ) The proliferation of NPCs was evaluated at 24-hour and 72-hour time points following treatments with bFGF or FGFR-agonist, using a CCK8 kit. ( B ) Serum-starved NPCs were placed in the upper chamber, while bFGF(20 ng/mL) and FGFR-agonist (40 nM) were included in the lower chamber for 24 h and stained, followed visualization under light microscopy. Scale bar = 100 μm. ( C ) The data from the Transwell assay are quantified to assess the impact of different treatments on NPC migration. Data are presented as mean ± SD (n = 6). ( D ) Representative images showing the undifferentiated NPCs (Nestin-positive) and differentiated neurons <t>(Tuj-1</t> positive) NPCs treated with bFGF, FGFR-agonist and Ctrl-oligo for 7 days and subjected to immunofluorescence staining. Scale bar = 100 μm. ( E ) The ratios of Nestin-positive cells and Tuj-1-positive cells are quantified against total cells (DAPI-positive). Data are presented as mean ± SD (n = 3), with **p < 0.001, as determined by unpaired t-tests. ( F ) Representative images of neurospheres generated by NPCs cultured in suspension for 10 days in the presence or absence of bFGF (20 ng/mL), FGFR-agonist (40 nM), or FGFR-agonist (200 nM). The scale bar = 100 μm. (G) Quantification of the changes in neurosphere volume over a 10-day culture period under various treatment conditions. Data are displayed as mean ± SD (n = 3), with **p < 0.0001, as determined by one-way ANOVA
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FGFR-agonist regulates cellular behaviors of NPCs. ( A ) The proliferation of NPCs was evaluated at 24-hour and 72-hour time points following treatments with bFGF or FGFR-agonist, using a CCK8 kit. ( B ) Serum-starved NPCs were placed in the upper chamber, while bFGF(20 ng/mL) and FGFR-agonist (40 nM) were included in the lower chamber for 24 h and stained, followed visualization under light microscopy. Scale bar = 100 μm. ( C ) The data from the Transwell assay are quantified to assess the impact of different treatments on NPC migration. Data are presented as mean ± SD (n = 6). ( D ) Representative images showing the undifferentiated NPCs (Nestin-positive) and differentiated neurons <t>(Tuj-1</t> positive) NPCs treated with bFGF, FGFR-agonist and Ctrl-oligo for 7 days and subjected to immunofluorescence staining. Scale bar = 100 μm. ( E ) The ratios of Nestin-positive cells and Tuj-1-positive cells are quantified against total cells (DAPI-positive). Data are presented as mean ± SD (n = 3), with **p < 0.001, as determined by unpaired t-tests. ( F ) Representative images of neurospheres generated by NPCs cultured in suspension for 10 days in the presence or absence of bFGF (20 ng/mL), FGFR-agonist (40 nM), or FGFR-agonist (200 nM). The scale bar = 100 μm. (G) Quantification of the changes in neurosphere volume over a 10-day culture period under various treatment conditions. Data are displayed as mean ± SD (n = 3), with **p < 0.0001, as determined by one-way ANOVA
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Image Search Results


Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.

Journal: Bioactive Materials

Article Title: A cell motility-based selective hydrogel enables rapid generation of nerve-repairing blood clots

doi: 10.1016/j.bioactmat.2026.05.015

Figure Lengend Snippet: Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.

Article Snippet: Then, the samples were fixed and stained with astrocyte marker GFAP (1:500, CST, Rabbit mAb #80788) and neuron marker Tuj-1 (1:200, HUABIO, SP06-00) to assess differentiation.

Techniques: Derivative Assay, Membrane, Staining, CCK-8 Assay, Immunostaining, Control, Migration

FGFR-agonist regulates cellular behaviors of NPCs. ( A ) The proliferation of NPCs was evaluated at 24-hour and 72-hour time points following treatments with bFGF or FGFR-agonist, using a CCK8 kit. ( B ) Serum-starved NPCs were placed in the upper chamber, while bFGF(20 ng/mL) and FGFR-agonist (40 nM) were included in the lower chamber for 24 h and stained, followed visualization under light microscopy. Scale bar = 100 μm. ( C ) The data from the Transwell assay are quantified to assess the impact of different treatments on NPC migration. Data are presented as mean ± SD (n = 6). ( D ) Representative images showing the undifferentiated NPCs (Nestin-positive) and differentiated neurons (Tuj-1 positive) NPCs treated with bFGF, FGFR-agonist and Ctrl-oligo for 7 days and subjected to immunofluorescence staining. Scale bar = 100 μm. ( E ) The ratios of Nestin-positive cells and Tuj-1-positive cells are quantified against total cells (DAPI-positive). Data are presented as mean ± SD (n = 3), with **p < 0.001, as determined by unpaired t-tests. ( F ) Representative images of neurospheres generated by NPCs cultured in suspension for 10 days in the presence or absence of bFGF (20 ng/mL), FGFR-agonist (40 nM), or FGFR-agonist (200 nM). The scale bar = 100 μm. (G) Quantification of the changes in neurosphere volume over a 10-day culture period under various treatment conditions. Data are displayed as mean ± SD (n = 3), with **p < 0.0001, as determined by one-way ANOVA

Journal: Biological Research

Article Title: Development of synthetic modulator enabling long-term propagation and neurogenesis of human embryonic stem cell-derived neural progenitor cells

doi: 10.1186/s40659-023-00471-0

Figure Lengend Snippet: FGFR-agonist regulates cellular behaviors of NPCs. ( A ) The proliferation of NPCs was evaluated at 24-hour and 72-hour time points following treatments with bFGF or FGFR-agonist, using a CCK8 kit. ( B ) Serum-starved NPCs were placed in the upper chamber, while bFGF(20 ng/mL) and FGFR-agonist (40 nM) were included in the lower chamber for 24 h and stained, followed visualization under light microscopy. Scale bar = 100 μm. ( C ) The data from the Transwell assay are quantified to assess the impact of different treatments on NPC migration. Data are presented as mean ± SD (n = 6). ( D ) Representative images showing the undifferentiated NPCs (Nestin-positive) and differentiated neurons (Tuj-1 positive) NPCs treated with bFGF, FGFR-agonist and Ctrl-oligo for 7 days and subjected to immunofluorescence staining. Scale bar = 100 μm. ( E ) The ratios of Nestin-positive cells and Tuj-1-positive cells are quantified against total cells (DAPI-positive). Data are presented as mean ± SD (n = 3), with **p < 0.001, as determined by unpaired t-tests. ( F ) Representative images of neurospheres generated by NPCs cultured in suspension for 10 days in the presence or absence of bFGF (20 ng/mL), FGFR-agonist (40 nM), or FGFR-agonist (200 nM). The scale bar = 100 μm. (G) Quantification of the changes in neurosphere volume over a 10-day culture period under various treatment conditions. Data are displayed as mean ± SD (n = 3), with **p < 0.0001, as determined by one-way ANOVA

Article Snippet: After 10 days of differentiation, the cells were fixed and immunostained with specific antibodies against neuronal marker Tuj-1 (Abcam) and NPC marker Nestin (Abcam).

Techniques: Staining, Light Microscopy, Transwell Assay, Migration, Immunofluorescence, Generated, Cell Culture, Suspension

The potency for neurogenesis of long-term propagated NPCs by FGFR-agonist. ( A ) The influence of FGFR-agonist on proliferative capacity of the NPCs after 50 passages. NPCs maintained in FGFR-agonist were propagated for 50 passages and treated with either bFGF, FGFR-agonist or Ctrl-oligo for 72 h. The cell proliferation was assessed using the CCK8 assay. Data are depicted as mean ± SD (n = 5), with *p < 0.001 (one-way ANOVA). ( B ) Long-term propagated NPCs underwent different treatment regimens, including bFGF, FGFR-agonist, or NGF-induced differentiation, over a 10-day period. Following treatment, cells were fixed and analyzed via immunofluorescence. Nestin is represented through green fluorescence, while Tuj-1 is indicated by red fluorescence. Cell nuclei are counterstained with DAPI for contrast. Scale bar = 100 μm. Specific regions of interest (ROI), delineated by white-bordered boxes, are further magnified to provide a detailed view, accompanied by a zoom-in scale bar set at 10 μm

Journal: Biological Research

Article Title: Development of synthetic modulator enabling long-term propagation and neurogenesis of human embryonic stem cell-derived neural progenitor cells

doi: 10.1186/s40659-023-00471-0

Figure Lengend Snippet: The potency for neurogenesis of long-term propagated NPCs by FGFR-agonist. ( A ) The influence of FGFR-agonist on proliferative capacity of the NPCs after 50 passages. NPCs maintained in FGFR-agonist were propagated for 50 passages and treated with either bFGF, FGFR-agonist or Ctrl-oligo for 72 h. The cell proliferation was assessed using the CCK8 assay. Data are depicted as mean ± SD (n = 5), with *p < 0.001 (one-way ANOVA). ( B ) Long-term propagated NPCs underwent different treatment regimens, including bFGF, FGFR-agonist, or NGF-induced differentiation, over a 10-day period. Following treatment, cells were fixed and analyzed via immunofluorescence. Nestin is represented through green fluorescence, while Tuj-1 is indicated by red fluorescence. Cell nuclei are counterstained with DAPI for contrast. Scale bar = 100 μm. Specific regions of interest (ROI), delineated by white-bordered boxes, are further magnified to provide a detailed view, accompanied by a zoom-in scale bar set at 10 μm

Article Snippet: After 10 days of differentiation, the cells were fixed and immunostained with specific antibodies against neuronal marker Tuj-1 (Abcam) and NPC marker Nestin (Abcam).

Techniques: CCK-8 Assay, Immunofluorescence, Fluorescence