vegf  (Thermo Fisher)

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Dynamic Perfusion Culture of Human Outgrowth Endothelial Progenitor Cells on Demineralized Bone Matrix In Vitro

doi: 10.12659/MSM.897884

Figure Lengend Snippet: Expression of CD34, VE-cadherin, and VEGF protein under static culture and dynamic perfusion culture. (* p

Article Snippet: Relative mRNA levels of CD34/VE-cadherin/VEGF were quantified by quantitative reverse transcriptase real-time PCR (QRT-PCR) using cDNA obtained from the reverse transcription reactions as template, with a StepOne instrument (Applied Biosystems) and SYBR-Green PCR Master Mix (Applied Biosystems).

Techniques: Expressing

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Article Title: Dynamic Perfusion Culture of Human Outgrowth Endothelial Progenitor Cells on Demineralized Bone Matrix In Vitro

doi: 10.12659/MSM.897884

Figure Lengend Snippet: The influence of dynamic perfusion culture on CD34/VE-cadherin/VEGF mRNA expression (* p

Article Snippet: Relative mRNA levels of CD34/VE-cadherin/VEGF were quantified by quantitative reverse transcriptase real-time PCR (QRT-PCR) using cDNA obtained from the reverse transcription reactions as template, with a StepOne instrument (Applied Biosystems) and SYBR-Green PCR Master Mix (Applied Biosystems).

Techniques: Expressing

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF

doi: 10.1038/labinvest.2009.95

Figure Lengend Snippet: ( a–f ) Role of GLUT1 in VEGF-induced MC FN production. ( a ) Primary culture mouse MCs with the C57BL6 background were studied in culture with and without VEGF-A 165 peptide (2 ng/ml) for 48 h. VEGF-A 165 stimulated a two-fold increase in MC GLUT1

Article Snippet: Immunohistochemical staining with various antibodies including GLUT1 (1:400, Alpha Diagnostic International, San Antonio, TX, USA), VEGF (1:200, Lab Vision, CA, USA), tenascin, phospho-PKCα (p-PKCα), and PKCβ1 (all 1:100, Santa Cruz Biotechnology, CA, USA), fibronectin (FN) and laminin (both 1:100, Sigma-Aldrich, St Louis, MO, USA), collagen IV (1:100, Santa Cruz Biotechnology, against α-1, α-3, and α-5 chains), CD2AP (1:100, Abcam, Cambridge, MA, USA), nephrin and podocin (both 1:100, kind gifts from Dr L Holzman, University of Michigan) was conducted using a Vectastain Elite ABC Kit (Vector Laboratories, Burlingame, CA, USA) with some modifications.

Techniques:

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF

doi: 10.1038/labinvest.2009.95

Figure Lengend Snippet: ( a–d ) Glomerular gene expression and glucose uptake rates in FvbROP Os/+ and FvbROP +/+ mice. ( a ) Western analyses of glomerular GLUT1, VEGF, PKCβ1, and PKCα in FvbROP +/+ and FvbROP Os/+ mice at 4 weeks of age ( n = 3–4

Article Snippet: Immunohistochemical staining with various antibodies including GLUT1 (1:400, Alpha Diagnostic International, San Antonio, TX, USA), VEGF (1:200, Lab Vision, CA, USA), tenascin, phospho-PKCα (p-PKCα), and PKCβ1 (all 1:100, Santa Cruz Biotechnology, CA, USA), fibronectin (FN) and laminin (both 1:100, Sigma-Aldrich, St Louis, MO, USA), collagen IV (1:100, Santa Cruz Biotechnology, against α-1, α-3, and α-5 chains), CD2AP (1:100, Abcam, Cambridge, MA, USA), nephrin and podocin (both 1:100, kind gifts from Dr L Holzman, University of Michigan) was conducted using a Vectastain Elite ABC Kit (Vector Laboratories, Burlingame, CA, USA) with some modifications.

Techniques: Expressing, Mouse Assay, Western Blot

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF

doi: 10.1038/labinvest.2009.95

Figure Lengend Snippet: ( a–c ) Cyclic mechanical stretch induction of MC GLUT1 and VEGF expression. ( a ) GLUT1 protein levels were increased at 48 h of stretch, and remained elevated at 72 h (not shown). ( b ) VEGF protein expression was increased at 72h of stretch, but

Article Snippet: Immunohistochemical staining with various antibodies including GLUT1 (1:400, Alpha Diagnostic International, San Antonio, TX, USA), VEGF (1:200, Lab Vision, CA, USA), tenascin, phospho-PKCα (p-PKCα), and PKCβ1 (all 1:100, Santa Cruz Biotechnology, CA, USA), fibronectin (FN) and laminin (both 1:100, Sigma-Aldrich, St Louis, MO, USA), collagen IV (1:100, Santa Cruz Biotechnology, against α-1, α-3, and α-5 chains), CD2AP (1:100, Abcam, Cambridge, MA, USA), nephrin and podocin (both 1:100, kind gifts from Dr L Holzman, University of Michigan) was conducted using a Vectastain Elite ABC Kit (Vector Laboratories, Burlingame, CA, USA) with some modifications.

Techniques: Expressing

Journal: PLoS ONE

Article Title: C-Kit Promotes Growth and Migration of Human Cardiac Progenitor Cells via the PI3K-AKT and MEK-ERK Pathways

doi: 10.1371/journal.pone.0140798

Figure Lengend Snippet: c-kit activation promotes growth of human c-kit+ CPCs under serum starvation. A, Activation of c-kit by SCF in human c-kit+ CPCs. CPCs were either treated with SCF (100 ng/ml) alone for 10 minutes or co-treated with imatinib. Cell lysate was analyzed by Western blot for the indicated proteins. p-c-kit, phosphorylated (i.e., activated) c-kit. B, Effect of SCF on cell growth. CPCs were serum starved for 24 hr and treated with SCF. The number of cells remaining was counted at the indicated time points. C, Dose-response relationship between SCF and CPC growth. CPCs were serum starved for 24 hr followed by treatment with varying concentrations of SCF, and the number of cells remaining after 3 days was determined. D, Representative DAPI nuclear staining images of SCF-treated CPCs described in panel C. E, Comparison of SCF with bFGF and VEGF in promoting growth of CPCs. CPCs were serum starved for 24 hr and treated with SCF, bFGF, or VEGF either individually or in combination, and the number of cells were counted on days 5 and 9 of treatment. F, Human c-kit+ CPCs were transduced with lentivirus expressing mCherry (control) or c-kit. Cell lysates were obtained at 4 days post-viral transduction and immunoblotted for c-kit and α-tubulin (loading control). G, mCherry or c-kit-expressing CPCs were serum starved for 24 hr and cultured for 3 days in the presence (+) or absence (-) of SCF and/or imatinib as indicated. Cell viability was assessed using PrestoBlue TM as described. Values were normalized to the DMSO (vehicle) control. Values are presented as mean ± SEM. *, p

Article Snippet: For bFGF and VEGF treatments, CPCs were incubated with 50 ng/ml bFGF (Peprotech) or 20 ng/ml VEGF (Invitrogen) either alone or in combination with SCF as indicated.

Techniques: Activation Assay, Western Blot, Staining, Transduction, Expressing, Cell Culture

Journal: PLoS ONE

Article Title: C-Kit Promotes Growth and Migration of Human Cardiac Progenitor Cells via the PI3K-AKT and MEK-ERK Pathways

doi: 10.1371/journal.pone.0140798

Figure Lengend Snippet: c-kit activation promotes migration of CPCs. Boyden chamber assay. Human c-kit+ CPCs were plated in the upper chamber, and the indicated growth factors were used as a chemoattractant in the lower chamber. After 24 hr, the migrated cells were fixed, stained with propidium iodide, and counted. A, Comparison of the pro-migratory effect of SCF and VEGF. B, Representative images showing the cells that migrated towards the indicated growth factors. C, CPCs transduced with lentivirus expressing mCherry (control) or c-kit were compared for their chemotaxis towards SCF in the presence (+) or absence (-) of 0.5 mM imatinib. Values presented are mean ± SEM. *, p

Article Snippet: For bFGF and VEGF treatments, CPCs were incubated with 50 ng/ml bFGF (Peprotech) or 20 ng/ml VEGF (Invitrogen) either alone or in combination with SCF as indicated.

Techniques: Activation Assay, Migration, Boyden Chamber Assay, Staining, Transduction, Expressing, Chemotaxis Assay

Journal: BMC Cancer

Article Title: A potential small-molecule synthetic antilymphangiogenic agent norcantharidin inhibits tumor growth and lymphangiogenesis of human colonic adenocarcinomas through blocking VEGF-A,-C,-D/VEGFR-2,-3 “multi-points priming” mechanisms in vitro and in vivo

doi: 10.1186/s12885-015-1521-5

Figure Lengend Snippet: NCTD inhibits the expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 proteins/mRNAs of the in-situ colonic xenografts in vivo. a Western-blotting: the expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 proteins in NCTD, Sorafenib, or NCTD + Sorafenib group was significantly downregulated as compared to control group (* P

Article Snippet: For S-P staining, slides were treated according to the kit brochure (Jinmei Biotechnology Co., Ltd., Shanghai), added in order with primary antibody [rabbit anti-human monoclonal antibody VEGF-A (Santa Gruz), VEGF-C (Invitrogen), VEGF-D (Abcam, USA), VEGFR-2 (Cell Signaling, USA), VEGFR-3 (Cell Signaling), biotinylated anti-rabbit secondary, HRP logo Streptavidin and DAB solution, respectively.

Techniques: Expressing, In Situ, In Vivo, Western Blot

Journal: BMC Cancer

Article Title: A potential small-molecule synthetic antilymphangiogenic agent norcantharidin inhibits tumor growth and lymphangiogenesis of human colonic adenocarcinomas through blocking VEGF-A,-C,-D/VEGFR-2,-3 “multi-points priming” mechanisms in vitro and in vivo

doi: 10.1186/s12885-015-1521-5

Figure Lengend Snippet: The expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 proteins/mRNAs of HCACCs and the co-culture system and the effect of NCTD on expression of these proteins/ mRNAs by western blotting ( a and b ) and fluorescent quantitative RT-PCR ( c and d ) in vitro . a and b Protein expression by western blotting: the expression of VEGF-C, VEGF-D and VEGFR-3 proteins of the co-culture system was higher than those of alone HCACC culture (* P = 0.001), but there was no difference on VEGF-A and VEGFR-2 expression between alone HCACC culture and the co-culture system. After treatment with NCTD, mF4-31C1 or NCTD + mF4-31C1, the expression of VEGF-C, VEGF-D and VEGFR-3 proteins of the co-culture system was downregulated significantly as compared to control group (all * P

Article Snippet: For S-P staining, slides were treated according to the kit brochure (Jinmei Biotechnology Co., Ltd., Shanghai), added in order with primary antibody [rabbit anti-human monoclonal antibody VEGF-A (Santa Gruz), VEGF-C (Invitrogen), VEGF-D (Abcam, USA), VEGFR-2 (Cell Signaling, USA), VEGFR-3 (Cell Signaling), biotinylated anti-rabbit secondary, HRP logo Streptavidin and DAB solution, respectively.

Techniques: Expressing, Co-Culture Assay, Western Blot, Quantitative RT-PCR, In Vitro

Journal: BMC Cancer

Article Title: A potential small-molecule synthetic antilymphangiogenic agent norcantharidin inhibits tumor growth and lymphangiogenesis of human colonic adenocarcinomas through blocking VEGF-A,-C,-D/VEGFR-2,-3 “multi-points priming” mechanisms in vitro and in vivo

doi: 10.1186/s12885-015-1521-5

Figure Lengend Snippet: The expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 protein products of HCACCs and the co-culture system of each group and the effect of NCTD on expression of these protein products in vitro (S-P staining, magnification × 200). a The expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 protein products of HCACCs and the co-culture system of each group. The expression of VEGF-C, VEGF-D and VEGFR-3 protein products (brown staining in cytoplasm) of the co-culture system was higher than those of alone HCACC culture (* P = 0.001); but there is no difference on the expression of VEGF-A and VEGFR-2 protein products between alone HCACC culture and the co-culture system. b The inhibitory effect of NCTD on expression of these protein products of the co-culture system. The expression of VEGF-C, VEGF-D and VEGFR-3 protein products in NCTD, mF4-31C1 or NCTD + mF4-31C1 group was downregulated significantly as compared to control group (* P

Article Snippet: For S-P staining, slides were treated according to the kit brochure (Jinmei Biotechnology Co., Ltd., Shanghai), added in order with primary antibody [rabbit anti-human monoclonal antibody VEGF-A (Santa Gruz), VEGF-C (Invitrogen), VEGF-D (Abcam, USA), VEGFR-2 (Cell Signaling, USA), VEGFR-3 (Cell Signaling), biotinylated anti-rabbit secondary, HRP logo Streptavidin and DAB solution, respectively.

Techniques: Expressing, Co-Culture Assay, In Vitro, Staining