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PMID |
Sentence |
1 |
16581909
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Phylogenetic promoter fingerprints of known elements of the slit diaphragm complex identified the nephrin model in the promoter region of zonula occludens-1 (ZO-1).
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2 |
16581909
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Nephrin, ZO-1, and cadherin-5 mRNA showed stringent coexpression across a diverse set of human glomerular diseases.
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3 |
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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4 |
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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5 |
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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6 |
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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7 |
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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8 |
18772335
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VEGF-C reduced labeled albumin flux by 32.8%.
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9 |
18772335
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VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively.
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10 |
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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11 |
18772335
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These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.
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12 |
18772335
|
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).
|
13 |
18772335
|
Here we define VEGFR-3 expression in GEnC and investigate the effects of the ligand VEGF-C.
|
14 |
18772335
|
VEGF-C effects on trans-endothelial electrical resistance and albumin flux across GEnC monolayers were measured.
|
15 |
18772335
|
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.
|
16 |
18772335
|
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.
|
17 |
18772335
|
VEGF-C reduced labeled albumin flux by 32.8%.
|
18 |
18772335
|
VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively.
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19 |
18772335
|
VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin.
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20 |
18772335
|
These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.
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21 |
21653636
|
Western blot and immunofluorescence analysis showed that podocyte markers (nephrin, CD2AP, podocin, Wilms' tumor-1) and an endothelial-specific molecule (VE-cadherin) were not detectable in this cell line, whereas markers characteristic of mesangial cells (α-SMA, fibronectin, and PDGFβ-R) were strongly expressed.
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22 |
25859060
|
We previously provided evidence that an apparent decrease in nephrin, caused by tensin2-deficiencient states, leads to podocytopathy, albuminuria and eventually, chronic renal failure.
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23 |
25859060
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Herein, we examined the changes of glomerular ECs, with focus on the expression of PECAM-1 and VE-cadherin (EC-specific markers), or of α-SMA (myofibroblast marker) in this mouse model by histological methods.
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24 |
25859060
|
Compared with the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the reduced expression of PECAM-1, or of VE-cadherin, in glomerular area.
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25 |
25859060
|
We previously provided evidence that an apparent decrease in nephrin, caused by tensin2-deficiencient states, leads to podocytopathy, albuminuria and eventually, chronic renal failure.
|
26 |
25859060
|
Herein, we examined the changes of glomerular ECs, with focus on the expression of PECAM-1 and VE-cadherin (EC-specific markers), or of α-SMA (myofibroblast marker) in this mouse model by histological methods.
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27 |
25859060
|
Compared with the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the reduced expression of PECAM-1, or of VE-cadherin, in glomerular area.
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