Journal: Journal of Molecular Medicine (Berlin, Germany)

Article Title: Stable tumor vessel normalization with pO 2 increase and endothelial PTEN activation by inositol trispyrophosphate brings novel tumor treatment

doi: 10.1007/s00109-013-0992-6

Figure Lengend Snippet: ITPP reduces melanoma tumor growth and improves mice survival. a Effect of ITPP treatment on the kinetics of tumor growth measured by bioluminescence in treated and nontreated animals at days 18 and 24. Endpoint was fixed at 2 cm 3 ( n = 6 animals per group, one representative experiment out of N > 10, ** p < 0.001). b Comparison of tumor size, 23 days after B16F10LucGFP cells injection, showing reduced tumor growth in treated mice. Representative groups of five animals among groups of n = 10 animals. One experiment out of N ≥ 5 separate experiments. Insets illustrate the extreme size ranges (minimal and maximal) that tumor reached in nontreated compared to treated mice. c Mean size of the tumors in treated and non treated animals at day 23 ( n = 10 in each group; number of experiments N > 20, ** p < 0.001). d Magnetic resonance imaging of B16 F10 induced tumor. Morphological pulse sequence ( left ). Strong volume variation of the tumor (untreated/ITPP = 1163 mm 3 /121 mm 3 ) was observed by image analysis after volume reconstruction. One typical example out of n = 10/experimental group. MRA-TOF/saturation recovery pulse sequence ( right ): Necrotic areas appear darker. After ITPP treatment, their size decreased. One typical example out of n = 10/experimental group. e Analysis by flow cytometry of B16LucGFP cells in tumors. Luciferase was detected intracellularly by specific antibodies and labeled by PerCP-Cy7 antirabbit IgG confirming: the reduced growth of tumor cells in ITPP-treated mice (%) and counts by direct cytometry analysis. Cells were numbered on the basis of intracellular Luciferase detection ( n = 8; * p < 0.05) from dot plots or inset from histogram analysis for quantification of B16F10LucGFP in the tumor

Article Snippet: Labeled primary antibodies used were the following: antimouse-CD31-PE (rat Ig-G2a, eBioscience) or CD31-PerCP (rat IgG2a, R&D), -VEGF R1-PE (Rat IgG2b, R&D), -VEGF R2-PE (Rat IgG2a, R&D), -CXCR4-PE (Rat IgG2b, R&D), -CD45-PerCP (rat IgG2b, R&D) or CD45-PE-Cy7 (rat IgG2b, R&D), -CD34-A700 (rat IgG2a, R&D).

Techniques: Injection, Magnetic Resonance Imaging, Sequencing, Flow Cytometry, Luciferase, Labeling, Cytometry

Journal: Journal of extracellular vesicles

Article Title: Anti-angiogenesis triggers exosomes release from endothelial cells to promote tumor vasculogenesis.

doi: 10.1080/20013078.2019.1629865

Figure Lengend Snippet: Figure 3. Autophagy acts as an adjuvant to Flk1-dependent angiogenesis.

Article Snippet: The primary antibodies included those against CD34 (1:100; ab81289; Abcam), human CD31 (1:100; GB11063-1, Servicebio, China), mouse CD31 (1:100; GB11063-3, Servicebio), VEGFA (1:100; TA500289; Origene), Flk1 (1:100; #9698; Cell Signaling Technology), p-Flk1 (Tyr1175; 1:100; #19A10; Cell Signaling Technology), and LC3B (1:100; ab192890; Abcam).

Techniques: Adjuvant

Journal: Journal of extracellular vesicles

Article Title: Anti-angiogenesis triggers exosomes release from endothelial cells to promote tumor vasculogenesis.

doi: 10.1080/20013078.2019.1629865

Figure Lengend Snippet: Figure 4. Inhibition of VEGFR (Flk1) or autophagy releases VEGF-enriched exosomes from HUVECs.

Article Snippet: The primary antibodies included those against CD34 (1:100; ab81289; Abcam), human CD31 (1:100; GB11063-1, Servicebio, China), mouse CD31 (1:100; GB11063-3, Servicebio), VEGFA (1:100; TA500289; Origene), Flk1 (1:100; #9698; Cell Signaling Technology), p-Flk1 (Tyr1175; 1:100; #19A10; Cell Signaling Technology), and LC3B (1:100; ab192890; Abcam).

Techniques: Inhibition

Journal: Journal of extracellular vesicles

Article Title: Anti-angiogenesis triggers exosomes release from endothelial cells to promote tumor vasculogenesis.

doi: 10.1080/20013078.2019.1629865

Figure Lengend Snippet: Figure 7. VEGF levels and Flk1 activation by VEGF-enriched exosomes.

Article Snippet: The primary antibodies included those against CD34 (1:100; ab81289; Abcam), human CD31 (1:100; GB11063-1, Servicebio, China), mouse CD31 (1:100; GB11063-3, Servicebio), VEGFA (1:100; TA500289; Origene), Flk1 (1:100; #9698; Cell Signaling Technology), p-Flk1 (Tyr1175; 1:100; #19A10; Cell Signaling Technology), and LC3B (1:100; ab192890; Abcam).

Techniques: Activation Assay

Journal: Journal of Angiogenesis Research

Article Title: A role for Egfl7 during endothelial organization in the embryoid body model system

doi: 10.1186/2040-2384-2-4

Figure Lengend Snippet: Effect of Egfl7 knock-down on in vitro endothelial development . Cryosections of EBs at day 7 (a, b, f, g, k, l, p, q) and day 14 (c, d, h, i, m, n, r, s) were subjected to indirect IF using antibodies against CD31 plus collagen IV (a-d), CD31 plus VE-cadherin (f-i), CD31 plus claudin 5 (k-n), or CD31 plus Flk1 (p-s). Magnification used; (a-d, f-i, k-n) inserts show whole EBs at 20×, and large panels show detail at 63×, (p-s) panels show EBs at 20×, (e, j, o, t) panels show whole EB IgG controls at 20× (arrows, CD31+ cords; arrowheads, CD31+ sheets). Images were acquired using a confocal laser microscope (Leica Microsystems; a-o) or an Axioplan 2 imaging microscope (Carl Zeiss; p-t).

Article Snippet: Sequential double-staining was carried out with the anti-CD31 antibody first, and antibodies were used as follows; rat anti-mouse CD31, 5 μg/ml (BD Biosciences), goat anti-mouse Flk1, 4 μg/ml (Santa Cruz), rabbit anti-mouse Collagen IV, 5 μg/ml (Chemicon), goat anti-mouse VE-Cadherin, 5 μg/ml (R&D Systems), rabbit anti-mouse Claudin-5, 2.5 μg/ml (Invitrogen), rabbit anti-mouse Ki67, 1.5 μg/ml (Abcam), rabbit anti-mouse Annexin-V, 2.5 μg/ml (Abcam).

Techniques: Knockdown, In Vitro, Microscopy, Imaging

Journal: Cancers

Article Title: Upregulation of Cell Surface Glycoproteins in Correlation with KSHV LANA in the Kaposi Sarcoma Tumor Microenvironment

doi: 10.3390/cancers15072171

Figure Lengend Snippet: Six of the potential markers are robustly translated into protein within KS tumors. ( A – F ) Dual IF of the co-expression of LANA and the indicated potential KS biomarker. FLT4, KDR, UNC5A, ADAM12, CD34, and Prox-1 had robust expression in the KS lesions and were not exclusively detected in LANA-positive cells. ZP2 and OX40 were not detected at the protein level in KS lesions despite high transcriptomic expression. LANA is denoted as red, and the surface marker in question is green. Open yellow arrows indicate LANA-positive cells, and closed arrows indicate LANA-negative cells.

Article Snippet: The antibodies used for IHC were as follows: mouse anti-LANA (Leica, Deer Park, IL, USA, 1:100), rat anti-LANA (Abcam, Boston, MA, USA, 1:100), mouse-anti CD34 (Invitrogen, Boston, MA, USA 1:200), rabbit-anti Prox-1 (Abcam, 1:500), rabbit-anti KDR (ProteinTech, Rosemont, IL, USA, 1:1500), rabbit-anti FLT4 (Invitrogen, 1:800), rabbit-anti ADAM12 (Invitrogen, 1:500), rabbit-anti UNC5A (ProteinTech, 1:300), rabbit-anti OX40 (Novus, Centennial, CO, USA 1:500), rabbit-anti ZP2 (Invitrogen, 1:5000).

Techniques: Expressing, Biomarker Discovery, Marker

Journal: Cancers

Article Title: Upregulation of Cell Surface Glycoproteins in Correlation with KSHV LANA in the Kaposi Sarcoma Tumor Microenvironment

doi: 10.3390/cancers15072171

Figure Lengend Snippet: Dual IF of KSHV-infected L1T2 and uninfected TIVE cells shows the expression of KDR, FLT4, and UNC5a but not ADAM12 or the endothelial markers. ( A – L ) Dual IF of the co-expression of LANA and the indicated potential KS biomarker. ADAM12, CD34, and Prox-1 were not detected in either cell line. FLT4, KDR, and UNC5A had low to moderate expression in the KS lesions and were not exclusively detected in LANA-positive cells. LANA is denoted as red, and the surface marker in question is green. Open yellow arrows indicate LANA-positive cells, and closed arrows indicate LANA-negative cells. Images were acquired at 20X magnification.

Article Snippet: The antibodies used for IHC were as follows: mouse anti-LANA (Leica, Deer Park, IL, USA, 1:100), rat anti-LANA (Abcam, Boston, MA, USA, 1:100), mouse-anti CD34 (Invitrogen, Boston, MA, USA 1:200), rabbit-anti Prox-1 (Abcam, 1:500), rabbit-anti KDR (ProteinTech, Rosemont, IL, USA, 1:1500), rabbit-anti FLT4 (Invitrogen, 1:800), rabbit-anti ADAM12 (Invitrogen, 1:500), rabbit-anti UNC5A (ProteinTech, 1:300), rabbit-anti OX40 (Novus, Centennial, CO, USA 1:500), rabbit-anti ZP2 (Invitrogen, 1:5000).

Techniques: Infection, Expressing, Biomarker Discovery, Marker

Journal: Cancers

Article Title: Upregulation of Cell Surface Glycoproteins in Correlation with KSHV LANA in the Kaposi Sarcoma Tumor Microenvironment

doi: 10.3390/cancers15072171

Figure Lengend Snippet: Dual IF demonstrating the colocalization of markers and LANA in mouse xenograft tissue. ( A – F ) Dual IF of the co-expression of LANA and the indicated potential KS biomarker. FLT4, KDR, UNC5A, and ADAM12 had robust expression in the KS lesions and were not exclusively detected in LANA-positive cells. CD34 and Prox-1 were not detected at the protein level. LANA is denoted as red, and the surface marker in question is green. Images were acquired at 20X magnification.

Article Snippet: The antibodies used for IHC were as follows: mouse anti-LANA (Leica, Deer Park, IL, USA, 1:100), rat anti-LANA (Abcam, Boston, MA, USA, 1:100), mouse-anti CD34 (Invitrogen, Boston, MA, USA 1:200), rabbit-anti Prox-1 (Abcam, 1:500), rabbit-anti KDR (ProteinTech, Rosemont, IL, USA, 1:1500), rabbit-anti FLT4 (Invitrogen, 1:800), rabbit-anti ADAM12 (Invitrogen, 1:500), rabbit-anti UNC5A (ProteinTech, 1:300), rabbit-anti OX40 (Novus, Centennial, CO, USA 1:500), rabbit-anti ZP2 (Invitrogen, 1:5000).

Techniques: Expressing, Biomarker Discovery, Marker