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PMID |
Sentence |
1 |
12819328
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Regions examined were at human chromosome 10p,10q (orthologous to the rat renal susceptibility Rf-1 locus), and at NPHS1 (nephrin), CD2AP, Wilms tumor (WT1), and NPHS2 (podocin) loci.
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2 |
12819328
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We have excluded linkage with candidate regions for nephrin, CD2AP, WT1, and podocin in this sample.
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3 |
12819328
|
Regions examined were at human chromosome 10p,10q (orthologous to the rat renal susceptibility Rf-1 locus), and at NPHS1 (nephrin), CD2AP, Wilms tumor (WT1), and NPHS2 (podocin) loci.
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4 |
12819328
|
We have excluded linkage with candidate regions for nephrin, CD2AP, WT1, and podocin in this sample.
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5 |
15509792
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Therefore, to investigate the mechanism of Wt1 R394W-induced renal failure, the expression of genes whose deletion leads to glomerulosclerosis (NPHS1, NPHS2, and CD2AP) was quantitated.
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6 |
15509792
|
In mutant kidneys, NPHS1 and NPHS2 were only moderately downregulated (25 to 30%) at birth but not at 2 or 4 months.
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7 |
15509792
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Two other genes implicated in glomerulosclerosis, TGFB1 and IGF1, were upregulated at 2 months and at 2 and 4 months, respectively.
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8 |
15509792
|
However, the data do suggest that Wt1 R394W-induced glomerulosclerosis may be independent of downregulation of the genes for NPHS1, NPHS2, CD2AP, and podocalyxin and may involve other genes yet to be implicated in renal failure.
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9 |
15509792
|
Therefore, to investigate the mechanism of Wt1 R394W-induced renal failure, the expression of genes whose deletion leads to glomerulosclerosis (NPHS1, NPHS2, and CD2AP) was quantitated.
|
10 |
15509792
|
In mutant kidneys, NPHS1 and NPHS2 were only moderately downregulated (25 to 30%) at birth but not at 2 or 4 months.
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11 |
15509792
|
Two other genes implicated in glomerulosclerosis, TGFB1 and IGF1, were upregulated at 2 months and at 2 and 4 months, respectively.
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12 |
15509792
|
However, the data do suggest that Wt1 R394W-induced glomerulosclerosis may be independent of downregulation of the genes for NPHS1, NPHS2, CD2AP, and podocalyxin and may involve other genes yet to be implicated in renal failure.
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13 |
15616033
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TERalb (%/h) was similar in normoalbuminuric and microalbuminuric group 1, 2, and 3 diabetic patients (medians: 14.1 vs. 14.4 vs. 15.7 vs. 14.9, respectively) (ANOVA, NS). mRNA expression of slit diaphragm proteins CD2AP, FAT, Actn 4, NPHS1, and NPHS2 was higher in normoalbuminuric patients than in microalbuminuric patients (groups 1, 2, and 3) (ANOVA, P < 0.001).
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14 |
16710349
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No change from base line values was observed as for hs-C-reactive protein and interleukin-6.
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15 |
16710349
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Real-time polymerase chain reaction measurement of mRNA SD proteins (CD2AP, FAT, Actn 4, NPHS1, and NPHS2) significantly increased in kidney biopsy specimens after simvastatin, but not cholestyramine treatment.
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16 |
17508916
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Hyperglycemia, elevated circulating fatty acids, inadequate local activation of renin angiotensin system, and chronic low grade inflammation are conditions that coexist in the CMS and DM2 that turn out to be deleterious for the beta-cell functioning and existance.
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17 |
17508916
|
Activation of the NADPH oxidase complex secondary to angiotensin II stimulation is of interest, as its pharmacological blockade has beneficial effects.
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18 |
17508916
|
New knowledge about the intimate mechanisms of oxidative-stress induced beta-cell failure will provide new therapeutic targets against CMS and DM2.
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19 |
17508916
|
Hyperglycemia, elevated circulating fatty acids, inadequate local activation of renin angiotensin system, and chronic low grade inflammation are conditions that coexist in the CMS and DM2 that turn out to be deleterious for the beta-cell functioning and existance.
|
20 |
17508916
|
Activation of the NADPH oxidase complex secondary to angiotensin II stimulation is of interest, as its pharmacological blockade has beneficial effects.
|
21 |
17508916
|
New knowledge about the intimate mechanisms of oxidative-stress induced beta-cell failure will provide new therapeutic targets against CMS and DM2.
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22 |
17804487
|
High glucose (HG; 25 mM) induces rounding of differentiated podocytes and changes in the distribution of F-actin but without quantitative changes in E-cadherin and the podocyte markers podocin, CD2AP, Neph1, or synaptopodin.
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23 |
17804487
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In these cells, BMP7 effectively activates smad5 (but not smad1) and raises p38 phosphorylation [which is also increased by transforming growth factor-beta (TGF-beta)].
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24 |
17804487
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HG as well as TGF-beta raise caspase-3 activity, increase apoptosis, and reduce cell survival which is, in part, blocked by BMP7.
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25 |
17804487
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Knockdown and forced expression studies indicate that smad5 is required as well as sufficient for these actions of BMP7.
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26 |
17804487
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These findings indicate that BMP7 is a differentiation and survival factor for podocytes, requires smad5, and can reduce diabetic podocyte injury.
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27 |
23681557
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CD2-associated protein (CD2AP) is essential for podocyte function.
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