vascular endothelial cells Search Results


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Elabscience Biotechnology vegf
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Vegf, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology vegf a elsa kit
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Vegf A Elsa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology plasma human vegf
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Plasma Human Vegf, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology elisa kits
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Elisa Kits, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cusabio human vegf elisa kit
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Human Vegf Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cusabio vascular endothelial growth factor vegf
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Vascular Endothelial Growth Factor Vegf, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cusabio csb e04757r
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Csb E04757r, supplied by Cusabio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cusabio csb e04756m mice vegf elisa kit
Figure 2. mRNA expression levels of <t>VEGF</t> 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.
Csb E04756m Mice Vegf Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cusabio vegf b elisa kit
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 <t>ELISA.</t> 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.
Vegf B Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cusabio elisa
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 <t>ELISA.</t> 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.
Elisa, supplied by Cusabio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vascular+endothelial+cells/Pig+Vascular+Endothelial+cell+Growth+Factor%2CVEGF+ELISA+KIT/pmc07267862-85-11-13
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Cell Signaling Technology Inc vegf121
EMCN knockdown inhibits <t>VEGF121</t> 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
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Elabscience Biotechnology mouse vascular endothelial growth factor a vegfa kit
EMCN knockdown inhibits <t>VEGF121</t> 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
Mouse Vascular Endothelial Growth Factor A Vegfa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


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.

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 VEGF (E-EL-M1292c) was purchased from Elabscience Biotechnology Co., Ltd., Wuhan, China.

Techniques: Expressing, Standard Deviation

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.

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 VEGF (E-EL-M1292c) was purchased from Elabscience Biotechnology Co., Ltd., Wuhan, China.

Techniques: Immunohistochemical staining, Expressing, Immunohistochemistry, Staining, Standard Deviation

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.

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 VEGF (E-EL-M1292c) was purchased from Elabscience Biotechnology Co., Ltd., Wuhan, China.

Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Standard Deviation

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.

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 VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, MANN-WHITNEY, Comparison

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.

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 VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, Comparison

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.

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 VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay, Comparison, Isolation

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.

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 VEGF-B ELISA Kit (CSB-E04758h, CUSABIO) were used for the quantitative determination of TGF-α and VEGF-B levels.

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, Luciferase, Derivative Assay

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

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: VEGF121 (#8908) was obtained from Cell Signaling.

Techniques: Knockdown, Migration, Western Blot, Control

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

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: VEGF121 (#8908) was obtained from Cell Signaling.

Techniques: Phospho-proteomics, Activation Assay, Western Blot, Knockdown