# |
PMID |
Sentence |
1 |
26739892
|
Interestingly, inhibition of mPGES-1 with a small interfering RNA approach significantly attenuated ADR-induced downregualtion of podocin and nephrin.
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2 |
26739892
|
In agreement with the improvement of cell phenotypic alteration and apoptosis, the enhanced inflammatory markers of IL-1β and TNF-α were also significantly suppressed by mPGES-1 silencing.
|
3 |
26739892
|
Interestingly, inhibition of mPGES-1 with a small interfering RNA approach significantly attenuated ADR-induced downregualtion of podocin and nephrin.
|
4 |
26739892
|
In agreement with the improvement of cell phenotypic alteration and apoptosis, the enhanced inflammatory markers of IL-1β and TNF-α were also significantly suppressed by mPGES-1 silencing.
|
5 |
28879567
|
mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
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6 |
28879567
|
Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
|
7 |
28879567
|
In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
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8 |
28879567
|
In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
|
9 |
28879567
|
By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
|
10 |
28879567
|
Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
|
11 |
28879567
|
Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
|
12 |
28879567
|
More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
|
13 |
28879567
|
Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
|
14 |
28879567
|
Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
|
15 |
28879567
|
mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
|
16 |
28879567
|
Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
|
17 |
28879567
|
In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
|
18 |
28879567
|
In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
|
19 |
28879567
|
By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
|
20 |
28879567
|
Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
|
21 |
28879567
|
Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
|
22 |
28879567
|
More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
|
23 |
28879567
|
Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
|
24 |
28879567
|
Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
|
25 |
28879567
|
mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
|
26 |
28879567
|
Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
|
27 |
28879567
|
In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
|
28 |
28879567
|
In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
|
29 |
28879567
|
By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
|
30 |
28879567
|
Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
|
31 |
28879567
|
Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
|
32 |
28879567
|
More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
|
33 |
28879567
|
Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
|
34 |
28879567
|
Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
|
35 |
28879567
|
mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
|
36 |
28879567
|
Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
|
37 |
28879567
|
In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
|
38 |
28879567
|
In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
|
39 |
28879567
|
By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
|
40 |
28879567
|
Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
|
41 |
28879567
|
Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
|
42 |
28879567
|
More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
|
43 |
28879567
|
Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
|
44 |
28879567
|
Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
|
45 |
28879567
|
mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
|
46 |
28879567
|
Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
|
47 |
28879567
|
In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
|
48 |
28879567
|
In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
|
49 |
28879567
|
By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
|
50 |
28879567
|
Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
|
51 |
28879567
|
Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
|
52 |
28879567
|
More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
|
53 |
28879567
|
Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
|
54 |
28879567
|
Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
|
55 |
28879567
|
mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis.
|
56 |
28879567
|
Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis.
|
57 |
28879567
|
In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin.
|
58 |
28879567
|
In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment.
|
59 |
28879567
|
By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction.
|
60 |
28879567
|
Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade.
|
61 |
28879567
|
Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction.
|
62 |
28879567
|
More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines.
|
63 |
28879567
|
Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis.
|
64 |
28879567
|
Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy.
|