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PMID |
Sentence |
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10027397
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In normal skin and kidney, podoplanin colocalized with vascular endothelial growth factor receptor-3, the only other lymphatic marker presently available.
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2 |
10027397
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Complementary immunostaining of blood vessels was obtained with established endothelial markers (CD31, CD34, factor VIII-related antigen, and Ulex europaeus I lectin) as well as podocalyxin, another podocytic protein that is also localized in endothelia of blood vessels.
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15465483
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We have conducted a study of Foxc2 expression during mouse development using immunohistochemistry, and examined its expression in lymphatics compared to its paralog Foxc1 and to Vegfr-3, Prox1 and other lymphatic and blood vascular proteins.
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4 |
16209358
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Two members of the VEGF family, VEGF-C and VEGF-D are lymphangiogenic when activate VEGFR-3.
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5 |
16209358
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Finally, podoplanin is a glomerular podocyte membrane mucoprotein, which occurs together with VEGFR-3 in the lymphatic endothelium.
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6 |
16209358
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Two members of the VEGF family, VEGF-C and VEGF-D are lymphangiogenic when activate VEGFR-3.
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7 |
16209358
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Finally, podoplanin is a glomerular podocyte membrane mucoprotein, which occurs together with VEGFR-3 in the lymphatic endothelium.
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8 |
16525158
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Vascular endothelial growth factor (VEGF)-A is an autocrine survival factor for podocytes, which express two VEGF receptors, VEGF-R1 and VEGF-R3.
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9 |
16525158
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As VEGF-A is not a known ligand for VEGF-R3, the aim of this investigation was to examine whether VEGF-C, a known ligand for VEGF-R3, served a function in podocyte biology and whether this was VEGF-R3 dependent.
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16525158
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VEGF-C protein expression was localized to podocytes in contrast to VEGF-D, which was expressed in parietal epithelial cells.
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11 |
16525158
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Cytotoxicity experiments revealed that in hCIPs VEGF-C reduced cytotoxicity to 81.4+/-1.9% of serum-starved conditions (P<0.001, paired t-test, n=16), similar to VEGF-A (82.8+/-4.5% of serum-starved conditions, P<0.05, paired t-test).
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12 |
16525158
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VEGF-C was also shown to induce a 0.5+/-0.13-fold reduction in levels of MAPK phosphorylation compared with VEGF-A and VEGF-A-Mab treatment (P<0.05, ANOVA, n=4), yet had no effect on Akt phosphorylation.
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13 |
16525158
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Vascular endothelial growth factor (VEGF)-A is an autocrine survival factor for podocytes, which express two VEGF receptors, VEGF-R1 and VEGF-R3.
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14 |
16525158
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As VEGF-A is not a known ligand for VEGF-R3, the aim of this investigation was to examine whether VEGF-C, a known ligand for VEGF-R3, served a function in podocyte biology and whether this was VEGF-R3 dependent.
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15 |
16525158
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VEGF-C protein expression was localized to podocytes in contrast to VEGF-D, which was expressed in parietal epithelial cells.
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16 |
16525158
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Cytotoxicity experiments revealed that in hCIPs VEGF-C reduced cytotoxicity to 81.4+/-1.9% of serum-starved conditions (P<0.001, paired t-test, n=16), similar to VEGF-A (82.8+/-4.5% of serum-starved conditions, P<0.05, paired t-test).
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17 |
16525158
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VEGF-C was also shown to induce a 0.5+/-0.13-fold reduction in levels of MAPK phosphorylation compared with VEGF-A and VEGF-A-Mab treatment (P<0.05, ANOVA, n=4), yet had no effect on Akt phosphorylation.
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18 |
16773315
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TR-LE cells expressed lymphatic endothelial markers VEGFR-3 (vascular endothelial growth factor receptor), LYVE-1 (a lymphatic endothelial receptor), Prox-1 (a homeobox gene product), and podoplanin (a glomerular podocyte membrane mucoprotein), together with endothelial markers CD31, Tie-2, and VEGFR-2, whereas TR-BE cells expressed CD31, Tie-2, and VEGFR-2, but no lymphatic endothelial markers.
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18772335
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We have previously reported expression of vascular endothelial growth factor (VEGF)-A and -C in glomerular podocytes and actions of VEGF-A on glomerular endothelial cells (GEnC) that express VEGF receptor-2 (VEGFR-2).
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20 |
18772335
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Here we define VEGFR-3 expression in GEnC and investigate the effects of the ligand VEGF-C.
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21 |
18772335
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VEGF-C effects on trans-endothelial electrical resistance and albumin flux across GEnC monolayers were measured.
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22 |
18772335
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VEGF-C effects on intracellular calcium ([Ca2+]i) were measured using a fluorescence technique, receptor phosphorylation was examined by immunoprecipitation assays, and phosphorylation of myosin light chain-2 and VE-cadherin was assessed by blotting with phospho-specific antibodies.
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23 |
18772335
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GEnC expressed VEGFR-3 in tissue sections and culture, and VEGF-C increased trans-endothelial electrical resistance in a dose-dependent manner with a maximal effect at 120 minutes of 6.8 Omega whereas VEGF-C156S had no effect.
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24 |
18772335
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VEGF-C reduced labeled albumin flux by 32.8%.
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25 |
18772335
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VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively.
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26 |
18772335
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VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin.
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27 |
18772335
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These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.
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28 |
18772335
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We have previously reported expression of vascular endothelial growth factor (VEGF)-A and -C in glomerular podocytes and actions of VEGF-A on glomerular endothelial cells (GEnC) that express VEGF receptor-2 (VEGFR-2).
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29 |
18772335
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Here we define VEGFR-3 expression in GEnC and investigate the effects of the ligand VEGF-C.
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30 |
18772335
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VEGF-C effects on trans-endothelial electrical resistance and albumin flux across GEnC monolayers were measured.
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31 |
18772335
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VEGF-C effects on intracellular calcium ([Ca2+]i) were measured using a fluorescence technique, receptor phosphorylation was examined by immunoprecipitation assays, and phosphorylation of myosin light chain-2 and VE-cadherin was assessed by blotting with phospho-specific antibodies.
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32 |
18772335
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GEnC expressed VEGFR-3 in tissue sections and culture, and VEGF-C increased trans-endothelial electrical resistance in a dose-dependent manner with a maximal effect at 120 minutes of 6.8 Omega whereas VEGF-C156S had no effect.
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33 |
18772335
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VEGF-C reduced labeled albumin flux by 32.8%.
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34 |
18772335
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VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively.
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35 |
18772335
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VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin.
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36 |
18772335
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These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.
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37 |
18772335
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We have previously reported expression of vascular endothelial growth factor (VEGF)-A and -C in glomerular podocytes and actions of VEGF-A on glomerular endothelial cells (GEnC) that express VEGF receptor-2 (VEGFR-2).
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38 |
18772335
|
Here we define VEGFR-3 expression in GEnC and investigate the effects of the ligand VEGF-C.
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39 |
18772335
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VEGF-C effects on trans-endothelial electrical resistance and albumin flux across GEnC monolayers were measured.
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40 |
18772335
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VEGF-C effects on intracellular calcium ([Ca2+]i) were measured using a fluorescence technique, receptor phosphorylation was examined by immunoprecipitation assays, and phosphorylation of myosin light chain-2 and VE-cadherin was assessed by blotting with phospho-specific antibodies.
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41 |
18772335
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GEnC expressed VEGFR-3 in tissue sections and culture, and VEGF-C increased trans-endothelial electrical resistance in a dose-dependent manner with a maximal effect at 120 minutes of 6.8 Omega whereas VEGF-C156S had no effect.
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42 |
18772335
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VEGF-C reduced labeled albumin flux by 32.8%.
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43 |
18772335
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VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively.
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44 |
18772335
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VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin.
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45 |
18772335
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These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.
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46 |
19031946
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This was mainly due to the discovery of lymphatic endothelial cell (LEC)-specific markers, such as vascular endothelial growth factor receptor-3 (VEGFR-3), LYVE-1, Prox-1 and podoplanin.
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47 |
19031946
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The expression of podoplanin is induced by the homeobox gene Prox-1 and a specific endogenous receptor was identified on platelets.
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48 |
29397483
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Consistent with these findings, genes known to regulate vessel caliber (Apln, AplnR and Vegfr3) are significantly upregulated in A10ΔEC glomeruli.
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