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recombinant rat vegf  (R&D Systems)


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    R&D Systems recombinant rat vegf
    Repulsive guidance molecule a (RGMa) expression increased in human umbilical artery endothelial cells (HUAECs), human umbilical vein endothelial cells (HUVECs), and rat brain microvascular endothelial cells (RBMECs) stimulated with <t>VEGF.</t> (A,B) Endothelial cell (EC) migration distance was evaluated by scratch assay. ECs were treated with a dose curve of RGMa (500–3000 ng/ml), and images were taken at the beginning and 12 h. (C,D) ECs were treated with RGMa (2 µg/ml), and lysates were collected over a time course of 50 min. The amount of phosphorylated focal adhesion kinase (p-FAK) protein was visualized with western blot analysis. (E,F) ECs were treated with VEGF (50 ng/ml), and lysates were collected over a course of 120 min. p-FAK protein levels were visualized with western blot analysis. (G–I) Quantitative real-time polymerase chain reaction showed RGMa mRNA level was upregulated in HUAECs, HUVECs, and RBMECs exposed to VEGF (50 ng/ml) for 30 min. (J–L) RGMa protein levels were visualized in HUAECs, HUVECs, and RBMECs exposed to VEGF at 30 min by western blot analysis. Data in bar graphs represent the means ± SD of ≥4 independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, # VS 1500 ng/ml, ### P < 0.001.
    Recombinant Rat Vegf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 36 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/564-RV/Recombinant+Rat+VEGF+164+Protein%2C+CF/pmc05623191-124-10-16
    Average 90 stars, based on 36 article reviews
    recombinant rat vegf - by Bioz Stars, 2026-10
    90/100 stars

    Images

    1) Product Images from "Repulsive Guidance Molecule a Inhibits Angiogenesis by Downregulating VEGF and Phosphorylated Focal Adhesion Kinase In Vitro"

    Article Title: Repulsive Guidance Molecule a Inhibits Angiogenesis by Downregulating VEGF and Phosphorylated Focal Adhesion Kinase In Vitro

    Journal: Frontiers in Neurology

    doi: 10.3389/fneur.2017.00504

    Repulsive guidance molecule a (RGMa) expression increased in human umbilical artery endothelial cells (HUAECs), human umbilical vein endothelial cells (HUVECs), and rat brain microvascular endothelial cells (RBMECs) stimulated with VEGF. (A,B) Endothelial cell (EC) migration distance was evaluated by scratch assay. ECs were treated with a dose curve of RGMa (500–3000 ng/ml), and images were taken at the beginning and 12 h. (C,D) ECs were treated with RGMa (2 µg/ml), and lysates were collected over a time course of 50 min. The amount of phosphorylated focal adhesion kinase (p-FAK) protein was visualized with western blot analysis. (E,F) ECs were treated with VEGF (50 ng/ml), and lysates were collected over a course of 120 min. p-FAK protein levels were visualized with western blot analysis. (G–I) Quantitative real-time polymerase chain reaction showed RGMa mRNA level was upregulated in HUAECs, HUVECs, and RBMECs exposed to VEGF (50 ng/ml) for 30 min. (J–L) RGMa protein levels were visualized in HUAECs, HUVECs, and RBMECs exposed to VEGF at 30 min by western blot analysis. Data in bar graphs represent the means ± SD of ≥4 independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, # VS 1500 ng/ml, ### P < 0.001.
    Figure Legend Snippet: Repulsive guidance molecule a (RGMa) expression increased in human umbilical artery endothelial cells (HUAECs), human umbilical vein endothelial cells (HUVECs), and rat brain microvascular endothelial cells (RBMECs) stimulated with VEGF. (A,B) Endothelial cell (EC) migration distance was evaluated by scratch assay. ECs were treated with a dose curve of RGMa (500–3000 ng/ml), and images were taken at the beginning and 12 h. (C,D) ECs were treated with RGMa (2 µg/ml), and lysates were collected over a time course of 50 min. The amount of phosphorylated focal adhesion kinase (p-FAK) protein was visualized with western blot analysis. (E,F) ECs were treated with VEGF (50 ng/ml), and lysates were collected over a course of 120 min. p-FAK protein levels were visualized with western blot analysis. (G–I) Quantitative real-time polymerase chain reaction showed RGMa mRNA level was upregulated in HUAECs, HUVECs, and RBMECs exposed to VEGF (50 ng/ml) for 30 min. (J–L) RGMa protein levels were visualized in HUAECs, HUVECs, and RBMECs exposed to VEGF at 30 min by western blot analysis. Data in bar graphs represent the means ± SD of ≥4 independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, # VS 1500 ng/ml, ### P < 0.001.

    Techniques Used: Expressing, Migration, Wound Healing Assay, Western Blot, Real-time Polymerase Chain Reaction

    Repulsive guidance molecule a (RGMa) suppressed VEGF expression, phosphorylation of focal adhesion kinase (FAK), proliferation, migration, and tube formation in ECs. (A,B) Lysate was collected, and VEGF was detected by western blot in human umbilical artery endothelial cells (HUAECs) treated with RGMa (2 µg/ml); (C–E) ELISA kit assay showed VEGFA decreased in endothelial cell (EC)-culture supernatant exposed to RGMa compared with cell-culture supernatant from control group. (F–H) Cell proliferation was evaluated with cell-counting kit-8 and 5-ethynyl-2′-deoxyuridine (EdU) assays (I,J) . RGMa decreased proliferation of ECs stimulated and unstimulated with VEGF. (K,L) FAK (Tyr397) phosphorylation was measured with western blot in HUAECs treated with vehicle, RGMa (2 µg/ml), VEGF (50 ng/ml), or VEGF plus RGMa. (M–P) ECs were grown to 100% confluence, serum-starved overnight, wounded with a sterile pipette tip to remove cells, and treated with control, RGMa, VEGF, or VEGF plus RGMa. Photographs (40×) were taken at 12 h after injury. Wound closure of ≥3 wells was quantified and reported as mean ± SD. (Q–T) Migration activity of ECs treated with RGMa, VEGF, VEGF plus RGMa, or control was measured with transwell assay. Photographs (200×) were taken 18 h after treatment. (U–X) HUAECs were starved overnight, treated as indicated, and seeded into 96-well plates coated with Matrigel. Photographs (40×) were taken at 3 h after treatment. The number of tubes, tube area, and tube length were analyzed with Image J. Scale bar, 100 µm. Data shown are representative of experimental and quantitative results. N ≥ 4 independent experiments. Bars represent mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: Repulsive guidance molecule a (RGMa) suppressed VEGF expression, phosphorylation of focal adhesion kinase (FAK), proliferation, migration, and tube formation in ECs. (A,B) Lysate was collected, and VEGF was detected by western blot in human umbilical artery endothelial cells (HUAECs) treated with RGMa (2 µg/ml); (C–E) ELISA kit assay showed VEGFA decreased in endothelial cell (EC)-culture supernatant exposed to RGMa compared with cell-culture supernatant from control group. (F–H) Cell proliferation was evaluated with cell-counting kit-8 and 5-ethynyl-2′-deoxyuridine (EdU) assays (I,J) . RGMa decreased proliferation of ECs stimulated and unstimulated with VEGF. (K,L) FAK (Tyr397) phosphorylation was measured with western blot in HUAECs treated with vehicle, RGMa (2 µg/ml), VEGF (50 ng/ml), or VEGF plus RGMa. (M–P) ECs were grown to 100% confluence, serum-starved overnight, wounded with a sterile pipette tip to remove cells, and treated with control, RGMa, VEGF, or VEGF plus RGMa. Photographs (40×) were taken at 12 h after injury. Wound closure of ≥3 wells was quantified and reported as mean ± SD. (Q–T) Migration activity of ECs treated with RGMa, VEGF, VEGF plus RGMa, or control was measured with transwell assay. Photographs (200×) were taken 18 h after treatment. (U–X) HUAECs were starved overnight, treated as indicated, and seeded into 96-well plates coated with Matrigel. Photographs (40×) were taken at 3 h after treatment. The number of tubes, tube area, and tube length were analyzed with Image J. Scale bar, 100 µm. Data shown are representative of experimental and quantitative results. N ≥ 4 independent experiments. Bars represent mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: Expressing, Phospho-proteomics, Migration, Western Blot, Enzyme-linked Immunosorbent Assay, Cell Culture, Control, Cell Counting, Sterility, Transferring, Activity Assay, Transwell Assay

    Repulsive guidance molecule a (RGMa) inhibited angiogenesis in vitro via neogenin. (A) Human umbilical artery endothelial cells (HUAECs) were transfected with CRISPR/Cas9 neogenin knockout kit and purified with puromycin, then the result of neogenin knockout was validated with western blot. (B,C) HUAECs transfected with SgRNA or neogenin gRNA were treated with vehicle, RGMa, VEGF, or VEGF plus RGMa. The focal adhesion kinase (FAK) (Tyr397) phosphorylation was measured with western blot. (D–G) Migration and (H–K) tube formation of HUAECs transfected with SgRNA or neogenin gRNA were determined by scratch, transwell, and Matrigel tube-formation assays. The relative number of tubes, tube area, and tube length were analyzed with Image J. Scale bar, 100 µm. Data shown are representative of experimental and quantitative results. N ≥ 4 independent experiments. Bars represent mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: Repulsive guidance molecule a (RGMa) inhibited angiogenesis in vitro via neogenin. (A) Human umbilical artery endothelial cells (HUAECs) were transfected with CRISPR/Cas9 neogenin knockout kit and purified with puromycin, then the result of neogenin knockout was validated with western blot. (B,C) HUAECs transfected with SgRNA or neogenin gRNA were treated with vehicle, RGMa, VEGF, or VEGF plus RGMa. The focal adhesion kinase (FAK) (Tyr397) phosphorylation was measured with western blot. (D–G) Migration and (H–K) tube formation of HUAECs transfected with SgRNA or neogenin gRNA were determined by scratch, transwell, and Matrigel tube-formation assays. The relative number of tubes, tube area, and tube length were analyzed with Image J. Scale bar, 100 µm. Data shown are representative of experimental and quantitative results. N ≥ 4 independent experiments. Bars represent mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: In Vitro, Transfection, CRISPR, Knock-Out, Purification, Western Blot, Phospho-proteomics, Migration

    Unc5b is involved in the effect of repulsive guidance molecule a (RGMa) on phosphorylation of focal adhesion kinase (FAK), migration, and tube formation in human umbilical artery endothelial cells (HUAECs). (A) HUAECs were transfected with CRISPR/Cas9 Unc5b knockout kits and purified with puromycin, then the effect of Unc5b knockout was validated with western blot. (B,C) HUAECs transfected with SgRNA or Unc5b gRNA were treated with control, RGMa, VEGF, or VEGF plus RGMa. FAK (Tyr397) phosphorylation was measured with western blot. (D–G) Migration and (H–K) tube formation of HUAECs transfected with SgRNA or Unc5b gRNA were determined with scratch, transwell, and Matrigel tube-formation assays. The relative number of tubes, tube area, and tube length was analyzed with Image J. Scale bar, 100 µm. Data shown are representative of experimental and quantitative results. N ≥ 4 independent experiments. Bars represent mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: Unc5b is involved in the effect of repulsive guidance molecule a (RGMa) on phosphorylation of focal adhesion kinase (FAK), migration, and tube formation in human umbilical artery endothelial cells (HUAECs). (A) HUAECs were transfected with CRISPR/Cas9 Unc5b knockout kits and purified with puromycin, then the effect of Unc5b knockout was validated with western blot. (B,C) HUAECs transfected with SgRNA or Unc5b gRNA were treated with control, RGMa, VEGF, or VEGF plus RGMa. FAK (Tyr397) phosphorylation was measured with western blot. (D–G) Migration and (H–K) tube formation of HUAECs transfected with SgRNA or Unc5b gRNA were determined with scratch, transwell, and Matrigel tube-formation assays. The relative number of tubes, tube area, and tube length was analyzed with Image J. Scale bar, 100 µm. Data shown are representative of experimental and quantitative results. N ≥ 4 independent experiments. Bars represent mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: Phospho-proteomics, Migration, Transfection, CRISPR, Knock-Out, Purification, Western Blot, Control

    Repulsive guidance molecule a (RGMa) inhibited cytoskeleton reassembly, filopodia, and lamellipodia formation in human umbilical artery endothelial cells (HUAECs) via neogenin and Unc5b. Before the immunofluorescence experiment, HUAECs were treated with vehicle, RGMa, VEGF, or VEGF plus RGMa for 40 min. F-actin was stained with phalloidin conjugated with FITC and phosphorylated focal adhesion kinase (p-FAK) connected with primary antibody was labeled with Alexa Fluor 555 donkey anti-rabbit (H + L) secondary antibody. (A) Immunofluorescence showed the cytoskeleton (green) change and p-FAK (red) distribution. (B) Immunofluorescence showing the cytoskeleton change of HUAECs transfected with SgRNA or neogenin gRNA. (C) Immunofluorescence showed the cytoskeleton change of HUAECs transfected with SgRNA or Unc5b gRNA. The filopodia are indicated as sharp spikes (arrowhead), and lamellipodia (arrow) are indicated as flat intensive staining. The merged images are shown in the upper panels, and the amplified indicated areas are shown in the lower panel for different groups. Photographs were obtained with laser scanning confocal microscopy (Nikon, A1 + R, magnification 400×). Results shown are representative images of ≥4 independent experiments.
    Figure Legend Snippet: Repulsive guidance molecule a (RGMa) inhibited cytoskeleton reassembly, filopodia, and lamellipodia formation in human umbilical artery endothelial cells (HUAECs) via neogenin and Unc5b. Before the immunofluorescence experiment, HUAECs were treated with vehicle, RGMa, VEGF, or VEGF plus RGMa for 40 min. F-actin was stained with phalloidin conjugated with FITC and phosphorylated focal adhesion kinase (p-FAK) connected with primary antibody was labeled with Alexa Fluor 555 donkey anti-rabbit (H + L) secondary antibody. (A) Immunofluorescence showed the cytoskeleton (green) change and p-FAK (red) distribution. (B) Immunofluorescence showing the cytoskeleton change of HUAECs transfected with SgRNA or neogenin gRNA. (C) Immunofluorescence showed the cytoskeleton change of HUAECs transfected with SgRNA or Unc5b gRNA. The filopodia are indicated as sharp spikes (arrowhead), and lamellipodia (arrow) are indicated as flat intensive staining. The merged images are shown in the upper panels, and the amplified indicated areas are shown in the lower panel for different groups. Photographs were obtained with laser scanning confocal microscopy (Nikon, A1 + R, magnification 400×). Results shown are representative images of ≥4 independent experiments.

    Techniques Used: Immunofluorescence, Staining, Labeling, Transfection, Amplification, Confocal Microscopy

    Related Articles

    Binding Assay:

    Article Title: Pharmacodynamic and Antitumor Activity of BI 836880, a Dual Vascular Endothelial Growth Factor and Angiopoietin 2 Inhibitor, Alone and Combined with Programmed Cell Death Protein-1 Inhibition.
    Article Snippet: Other reagents were RMP1-14 (murine anti–PD-1 antibody; BioXCell; BE0146) and the corresponding isotype InVivoMAb Rat IgG2a (BioXCell; BE0089), bevacizumab (anti-VEGF antibody; Roche), and vatalanib [small-molecule tyrosine kinase inhibitor of VEGF receptor (VEGFR); MedChemExpress; HY-12018]. .. For the binding assays, the following commercial recombinant proteins were used: human VEGF165 (R&D Systems; 293-VE/CF), human VEGF121 (R&D Systems; 298-VERSUS/CF), rat VEGF164 (R&D Systems; 564-RV/CF), mouse VEGF164 (R&D Systems; 493- MV/CF), human VEGF-B (R&D Systems; 751-VE), human VEGF-C (R&D Systems; 2179-VC/CF), human VEGF-D (R&D Systems; 622- VD/CF), human placental growth factor (R&D Systems; 264-PG/CF), FLAG-tagged human ANG1 (Alexis Biochemicals), FLAG-tagged human ANG2 (Alexis Biochemicals), human TIE2-Fc (R&D Systems; 313-TI), and recombinant human ANG2 (R&D Systems; 623-AN). .. Also used were recombinant proteins produced by Boehringer Ingelheim: mouse, rat, and cynomolgus ANG2-fibrinogen-like domain (FLD) fragments, as well as monomeric ANG2-FLD, which consists of the C-terminal FLD domain of ANG2 and contains the key amino acid residues involved in its interaction with the receptor TIE2.

    Recombinant:

    Article Title: Pharmacodynamic and Antitumor Activity of BI 836880, a Dual Vascular Endothelial Growth Factor and Angiopoietin 2 Inhibitor, Alone and Combined with Programmed Cell Death Protein-1 Inhibition.
    Article Snippet: Other reagents were RMP1-14 (murine anti–PD-1 antibody; BioXCell; BE0146) and the corresponding isotype InVivoMAb Rat IgG2a (BioXCell; BE0089), bevacizumab (anti-VEGF antibody; Roche), and vatalanib [small-molecule tyrosine kinase inhibitor of VEGF receptor (VEGFR); MedChemExpress; HY-12018]. .. For the binding assays, the following commercial recombinant proteins were used: human VEGF165 (R&D Systems; 293-VE/CF), human VEGF121 (R&D Systems; 298-VERSUS/CF), rat VEGF164 (R&D Systems; 564-RV/CF), mouse VEGF164 (R&D Systems; 493- MV/CF), human VEGF-B (R&D Systems; 751-VE), human VEGF-C (R&D Systems; 2179-VC/CF), human VEGF-D (R&D Systems; 622- VD/CF), human placental growth factor (R&D Systems; 264-PG/CF), FLAG-tagged human ANG1 (Alexis Biochemicals), FLAG-tagged human ANG2 (Alexis Biochemicals), human TIE2-Fc (R&D Systems; 313-TI), and recombinant human ANG2 (R&D Systems; 623-AN). .. Also used were recombinant proteins produced by Boehringer Ingelheim: mouse, rat, and cynomolgus ANG2-fibrinogen-like domain (FLD) fragments, as well as monomeric ANG2-FLD, which consists of the C-terminal FLD domain of ANG2 and contains the key amino acid residues involved in its interaction with the receptor TIE2.

    Article Title: AMP-activated protein kinase is a key regulator of acute neurovascular permeability
    Article Snippet: .. Recombinant rat VEGF-A (165) was purchased from R&D Systems (Abingdon, United Kingdom). .. Bradykinin, sulforhodamine B, Evans Blue, SU-1498, SB203580, compound C, STO-609, L-N G -nitroarginine methyl ester (L-NAME), BAPTA-AM, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), A769662, diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate (DEANO) and 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) were purchased from MERCK (Dorset, United Kingdom).



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    Image Search Results


    Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

    Journal: Exploration of BioMat-X

    Article Title: Top2b regulates morphological and migratory properties of retinal progenitor cells in vivo and upon transplantable matrix substrates

    doi: 10.37349/ebmx.2025.101335

    Figure Lengend Snippet: Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

    Article Snippet: Approximately 600 μL of each growth factor vascular endothelial growth factor (VEGF; R&D Systems, Minneapolis, MN, USA, 564-RV), fibroblast growth factor-8 (FGF-8; Invitrogen, Carlsbad, CA, USA, PHG0184), and stromal derived factor 1-a (SDF-1a; Sigma Aldrich, St. Louis, MO, USA, SRP3276) was added to the bottom of separate transwell assays.

    Techniques: Cell Culture, Over Expression, Knockdown, Expressing, Derivative Assay

    Figure 4. Induction of VEGF (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 4. Induction of VEGF (A,B), angiogenic factors (C) or pro-inflammatory factors (D) in cultured cells in vitro. RAW264.7 cells, NIH3T3 cells or U937 cells were cultured in hypoxic condition (5% or 0.5%) for 8 h (A,C,D) or indicated time period (B). The induction of Vegf (A), angiogenic factors (C) or pro-inflammatory factors (D) was then examined by RT-PCR analyses (A,C,D, n = 6) and the secretion of VEGF by ELISA (B, n = 6). Data represents as Mean and S.E.M. Statistical analysis was done by a non-parametric Mann–Whitney test or by a Kruskal–Wallis test followed by a Steel test. *p < 0.05, **p < 0.01.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Cell Culture, In Vitro, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    Figure 5. Expression of VEGF in rupture-prone intracranial aneurysm (IA) lesions induced in rats. The images of immunofluorescent staining of IA lesions for VEGF (green), the marker for macrophages, CD68 (red), the marker for smooth muscle cell, α-smooth muscle actin (SMA, gray), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Magnified images corresponding to the square in the upper panels are shown in the lower panels. Scale bar: 50 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 5. Expression of VEGF in rupture-prone intracranial aneurysm (IA) lesions induced in rats. The images of immunofluorescent staining of IA lesions for VEGF (green), the marker for macrophages, CD68 (red), the marker for smooth muscle cell, α-smooth muscle actin (SMA, gray), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Magnified images corresponding to the square in the upper panels are shown in the lower panels. Scale bar: 50 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Expressing, Staining, Marker, Immunohistochemistry, Negative Control

    Figure 6. Expression of VEGF in human unruptured intracranial aneurysm (IA) lesions. The images of immunofluorescent staining of IA lesions for VEGF (green), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Scale bar: 50 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 6. Expression of VEGF in human unruptured intracranial aneurysm (IA) lesions. The images of immunofluorescent staining of IA lesions for VEGF (green), nuclear staining by DAPI (blue), and merged images are shown. The images from immunohistochemistry without a primary antibody were served as a negative control. Scale bar: 50 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Expressing, Staining, Immunohistochemistry, Negative Control

    Figure 7. VEGF-mediated induction of neovessels in subarachnoid space. The sheet for slow-release of VEGF or vehicle was placed on the right or the left of brain surface in the same rat (A) and the induction of vasa vasorum in subarachnoid space was examined. Asterisks indicate the sheets placed on brain surface. Scale bar: 1 mm. The macroscopic image of the brain surface (B) and the histopathological images from hematoxylin– eosin staining from specimen of vehicle- or VEGF-treated side (C) are shown. Dotted circles in (B) indicate the region where the sheet was placed. Noted the reddish appearance only in the VEGF-treated side indicating the induction of neovessels. Magnified images corresponding to the square in the left panels in (C) are shown on the right. Arrows indicate the neovessels induced in subarachnoid space. Scale bar: 50 μm. The images of immunofluorescent staining for the marker for smooth muscle cell, α-smooth muscle actin (SMA, red), nuclear staining by DAPI (blue), and merged images are shown in (D). Magnified images corresponding to the squares in the left panels are shown on the right. Scale bar: 100 μm.

    Journal: Scientific reports

    Article Title: Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

    doi: 10.1038/s41598-023-32001-z

    Figure Lengend Snippet: Figure 7. VEGF-mediated induction of neovessels in subarachnoid space. The sheet for slow-release of VEGF or vehicle was placed on the right or the left of brain surface in the same rat (A) and the induction of vasa vasorum in subarachnoid space was examined. Asterisks indicate the sheets placed on brain surface. Scale bar: 1 mm. The macroscopic image of the brain surface (B) and the histopathological images from hematoxylin– eosin staining from specimen of vehicle- or VEGF-treated side (C) are shown. Dotted circles in (B) indicate the region where the sheet was placed. Noted the reddish appearance only in the VEGF-treated side indicating the induction of neovessels. Magnified images corresponding to the square in the left panels in (C) are shown on the right. Arrows indicate the neovessels induced in subarachnoid space. Scale bar: 50 μm. The images of immunofluorescent staining for the marker for smooth muscle cell, α-smooth muscle actin (SMA, red), nuclear staining by DAPI (blue), and merged images are shown in (D). Magnified images corresponding to the squares in the left panels are shown on the right. Scale bar: 100 μm.

    Article Snippet: :(0123456789) Scientific Reports | (2023) 13:5545 | https://doi.org/10.1038/s41598-023-32001-z slow-release of VEGF was placed on the brain surface (MedGel II from Nitta-gelatin (♯PI9, Osaka Japan) and recombinant human VEGF (1 μg/head, #564-RV-010/CF, lot #CWC0620081) from R&D systems, Inc. (Minneapolis, MN) resolved in phosphate buffered saline containing 0.1% human serum albumin (#A1653-5G, lot #SLBG2676V, Sigma)).

    Techniques: Staining, Marker