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Image Search Results
Journal: Molecular medicine reports
Article Title: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.
doi: 10.3892/mmr.2018.8980
Figure Lengend Snippet: Figure 2. mRNA expression levels of VEGF and MMP‑13 in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Relative mRNA expression levels of VEGF in the medial articular cartilage. (B) Relative mRNA expression levels of MMP‑13 in the medial articular cartilage. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; MMP‑13, matrix metalloproteinase‑13; Th, thalidomide; VEGF, vascular endothelial growth factor.
Article Snippet: An ELISA kit of
Techniques: Expressing, Standard Deviation
Journal: Molecular medicine reports
Article Title: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.
doi: 10.3892/mmr.2018.8980
Figure Lengend Snippet: Figure 3. Immunohistochemical analysis of VEGF expression in the knee articular cartilage of mice among the Sham, Dmm and Dmm+Th groups (n=4 in each group). (A) Immunohistochemistry staining of VEGF in the articular cartilage of the medial tibial plateau (magnification, x400, scale bar=100 µm). (B) Quantification of VEGF positive cells, based on the results of immunohistochemistry staining. The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; Th, thalidomide; VEGF, vascular endothelial growth factor.
Article Snippet: An ELISA kit of
Techniques: Immunohistochemical staining, Expressing, Immunohistochemistry, Staining, Standard Deviation
Journal: Molecular medicine reports
Article Title: Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.
doi: 10.3892/mmr.2018.8980
Figure Lengend Snippet: Figure 5. ELISA analysis of serum VEGF concentration of mice among the Sham, Dmm and Dmm+Th groups (n=8 in each group). The values are presented as the mean ± standard deviation. *P<0.05 compared with the Sham group; #P<0.05 compared with the Dmm group. Dmm, destabilization of the medial meniscus; Th, thalidomide; VEGF, vascular endothelial growth factor.
Article Snippet: An ELISA kit of
Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Standard Deviation
Journal: Neurology® Neuroimmunology & Neuroinflammation
Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis
doi: 10.1212/NXI.0000000000001043
Figure Lengend Snippet: TGF-α (A, B) and VEGF-B (C, D) levels as well as AHR agonistic activity (G, H) in serum samples of patients with RRMS in remission (n = 98), SPMS (n = 44), PPMS (n = 36), and their respective controls (A, C, E, G: n = 43; B, D, F, H: n = 16) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (E, F) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using nonparametric tests (Mann-Whitney test and Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons). **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; MS = multiple sclerosis; PPMS = primary progressive MS; RRMS = relapsing-remitting MS; SPMS = secondary progressive MS; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.
Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and
Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, MANN-WHITNEY, Comparison
Journal: Neurology® Neuroimmunology & Neuroinflammation
Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis
doi: 10.1212/NXI.0000000000001043
Figure Lengend Snippet: TGF-α (A) and VEGF-B (B) levels as well as AHR agonistic activity (D) were assessed in serum samples of patients with RRMS in remission (n = 98), RRMS during relapse (n = 54), and controls (n = 44). TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (C) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using the nonparametric Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons. **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.
Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and
Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, Comparison
Journal: Neurology® Neuroimmunology & Neuroinflammation
Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis
doi: 10.1212/NXI.0000000000001043
Figure Lengend Snippet: TGF-α (A) and VEGF-B (B) levels as well as AHR agonistic activity (D) were assessed in serum samples of patients with RRMS in remission (n = 98), CIS (n = 20), and controls (n = 44). TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio (C) was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are means of duplicate measurements. Lines represent median and interquartile range. Significance levels were derived using the nonparametric Kruskal-Wallis test with the Dunn multiple comparison test correcting for multiple comparisons. **** p < 0.0001, *** p < 0.001, ** p < 0.001, * p < 0.01, and ns = nonsignificant. AHR = aryl hydrocarbon receptor; CIS = clinically isolated syndrome; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.
Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and
Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, Comparison, Isolation
Journal: Neurology® Neuroimmunology & Neuroinflammation
Article Title: The Aryl Hydrocarbon Receptor–Dependent TGF-α/VEGF-B Ratio Correlates With Disease Subtype and Prognosis in Multiple Sclerosis
doi: 10.1212/NXI.0000000000001043
Figure Lengend Snippet: TGF-α/VEGF-B ratio (A) and AHR agonistic activity (B) in serum samples of patients with RRMS in remission (n = 98) were assessed. TGF-α and VEGF-B levels were measured in pg/mL using a human TGF-α or VEGF-B ELISA. TGF-α/VEGF-B ratio was determined by dividing TGF-α levels by VEGF-B levels. An AHR ligand–sensitive luciferase assay was used. Relative activity was calculated by dividing firefly luciferase activity (pGud-Luc) by Renilla luciferase activity (pTK-Renilla). Values are presented as means of duplicate measurements. Line shows linear regression of the TGF-α/VEGF-B ratio or AHR agonistic activity and patients' EDSS. Significance levels were derived using Spearman correlation analysis (A: Spearman r = −0.2427; R 2 = 0.059; B: Spearman r = −0.2433; R 2 = 0.059). AHR = aryl hydrocarbon receptor; EDSS = Expanded Disability Status Scale; RRMS = relapsing-remitting multiple sclerosis; TGF-α = transforming growth factor alpha; VEGF-B = vascular endothelial growth factor B.
Article Snippet: Commercial TGF-α ELISA Kit (EHTGF-Α, Thermo Scientific) and
Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay
Journal: Cell Communication and Signaling : CCS
Article Title: Endomucin selectively regulates vascular endothelial growth factor receptor-2 endocytosis through its interaction with AP2
doi: 10.1186/s12964-024-01606-w
Figure Lengend Snippet: EMCN knockdown inhibits VEGF121 induced VEGFR2 internalization and HRECs migration similar to VEGF165. A Both VEGF165 (10 ng/ml)- and VEGF121 (7.29 ng/ml)-induced migration were inhibited with EMCN knockdown. Quantification of cell migration by image analysis is shown (left). Student-t test was used for comparisons between groups. * P < 0.05, ** P < 0.01, n = 10. Representative images of each group at time zero (white dashed line) and 15 h time (yellow dashed line) points. The scale bar represents 500 µm. B Schematic representation of VEGFA isoforms, VEGF165 and VEGF121. C HRECs were treated with siEMCN stimulated with VEGF121 (7.29 ng/ml) for a time course of up to 120 min. VEGF121 induced significant VEGFR2 endocytosis after 60 min of stimulation, except when EMCN was knockdown. One-way ANOVA was used for comparation within group. Student-t test was used for comparation between siNT and siEMCN at the same time point. # P < 0.05, * P < 0.05, *** P < 0.001, **** P < 0.0001, n = 3. D Representative image of the western blot for VEGFR2 internalization in both siNT and siEMCN groups. CD31 was blotted as cell surface fraction loading control
Article Snippet:
Techniques: Knockdown, Migration, Western Blot, Control
Journal: Cell Communication and Signaling : CCS
Article Title: Endomucin selectively regulates vascular endothelial growth factor receptor-2 endocytosis through its interaction with AP2
doi: 10.1186/s12964-024-01606-w
Figure Lengend Snippet: Depletion of EMCN reduces the phosphorylation of FAK and Src following VEGFR2 activation. A Western blot image of p-VEGFR2, total VEGFR2, p-Src, total Src, p-FAK, total FAK, p-ERK1/2, total ERK1/2, and tubulin probing for a VEGF121 stimulation time course with and without EMCN. An equal quantity of protein was loaded into each well. B Densitometric analysis of western blot data demonstrated that knockdown of EMCN did not alter VEGF121-induced VEGFR2 activation. n = 3. C Western blot analysis demonstrated that VEGF121 activation of FAK at 10 min. D and Src at 10 min was diminished E whereas ERK activation was not affected by EMCN knockdown. One-way ANOVA analysis was used for comparation between different time points within group. Student-t test was used for comparation between siNT and siEMCN at the same time point. Statistical analysis. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 n ≥ 3
Article Snippet:
Techniques: Phospho-proteomics, Activation Assay, Western Blot, Knockdown