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PMID |
Sentence |
1 |
28211114
|
The old rats exhibited a dysregulation of the expression of proteins related to oxidative stress and inflammation in the kidneys, and MLB administration significantly reduced the protein expression of major subunits of nicotinamide adenine dinucleotide phosphate oxidase (Nox4 and p22phox ), phospho-p38, nuclear factor-kappa B p65, cyclooxygenase-2, and inducible nitric oxide synthase.
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2 |
28211114
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In addition, MLB-treated old rats showed lower levels of senescence-related proteins such as p16, ADP-ribosylation factor 6, p53, and p21 through effects on the mitogen-activated protein kinase pathway.
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3 |
28880939
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ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
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4 |
28880939
|
In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase.
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5 |
28880939
|
We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell.
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6 |
28880939
|
We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain.
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7 |
28880939
|
ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity.
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8 |
28880939
|
Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
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9 |
28880939
|
ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
|
10 |
28880939
|
In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase.
|
11 |
28880939
|
We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell.
|
12 |
28880939
|
We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain.
|
13 |
28880939
|
ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity.
|
14 |
28880939
|
Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
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15 |
28880939
|
ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
|
16 |
28880939
|
In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase.
|
17 |
28880939
|
We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell.
|
18 |
28880939
|
We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain.
|
19 |
28880939
|
ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity.
|
20 |
28880939
|
Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
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21 |
28880939
|
ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
|
22 |
28880939
|
In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase.
|
23 |
28880939
|
We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell.
|
24 |
28880939
|
We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain.
|
25 |
28880939
|
ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity.
|
26 |
28880939
|
Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
|
27 |
28880939
|
ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
|
28 |
28880939
|
In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase.
|
29 |
28880939
|
We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell.
|
30 |
28880939
|
We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain.
|
31 |
28880939
|
ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity.
|
32 |
28880939
|
Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
|
33 |
28880939
|
ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
|
34 |
28880939
|
In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase.
|
35 |
28880939
|
We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell.
|
36 |
28880939
|
We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain.
|
37 |
28880939
|
ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity.
|
38 |
28880939
|
Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
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39 |
31206670
|
ADP-ribosylation factor 6 (Arf6) is a small GTPase with pleiotropic effects and has previously been shown to regulate ATP-binding cassette transporter 1 (ABCA1) recycling, and thus, cholesterol homeostasis.
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40 |
31206670
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To investigate the role of Arf6 in cholesterol modulation in podocytes, the effect of Arf6 on the regulation of the cholesterol transporter ABCA1 was studied in podocytes in vivo and in vitro.
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41 |
31206670
|
Arf6 knockdown could cause ABCA1 recycling disorders, and thus, further aggravate cholesterol accumulation in podocytes under high-glucose (HG) conditions.
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42 |
31206670
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Our results demonstrate that HG-induced cholesterol accumulation and cellular injury in podocytes may be related to the recycling disorder of ABCA1 caused by the downexpression of Arf6 in DKD.
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43 |
31206670
|
ADP-ribosylation factor 6 (Arf6) is a small GTPase with pleiotropic effects and has previously been shown to regulate ATP-binding cassette transporter 1 (ABCA1) recycling, and thus, cholesterol homeostasis.
|
44 |
31206670
|
To investigate the role of Arf6 in cholesterol modulation in podocytes, the effect of Arf6 on the regulation of the cholesterol transporter ABCA1 was studied in podocytes in vivo and in vitro.
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45 |
31206670
|
Arf6 knockdown could cause ABCA1 recycling disorders, and thus, further aggravate cholesterol accumulation in podocytes under high-glucose (HG) conditions.
|
46 |
31206670
|
Our results demonstrate that HG-induced cholesterol accumulation and cellular injury in podocytes may be related to the recycling disorder of ABCA1 caused by the downexpression of Arf6 in DKD.
|
47 |
31206670
|
ADP-ribosylation factor 6 (Arf6) is a small GTPase with pleiotropic effects and has previously been shown to regulate ATP-binding cassette transporter 1 (ABCA1) recycling, and thus, cholesterol homeostasis.
|
48 |
31206670
|
To investigate the role of Arf6 in cholesterol modulation in podocytes, the effect of Arf6 on the regulation of the cholesterol transporter ABCA1 was studied in podocytes in vivo and in vitro.
|
49 |
31206670
|
Arf6 knockdown could cause ABCA1 recycling disorders, and thus, further aggravate cholesterol accumulation in podocytes under high-glucose (HG) conditions.
|
50 |
31206670
|
Our results demonstrate that HG-induced cholesterol accumulation and cellular injury in podocytes may be related to the recycling disorder of ABCA1 caused by the downexpression of Arf6 in DKD.
|
51 |
31206670
|
ADP-ribosylation factor 6 (Arf6) is a small GTPase with pleiotropic effects and has previously been shown to regulate ATP-binding cassette transporter 1 (ABCA1) recycling, and thus, cholesterol homeostasis.
|
52 |
31206670
|
To investigate the role of Arf6 in cholesterol modulation in podocytes, the effect of Arf6 on the regulation of the cholesterol transporter ABCA1 was studied in podocytes in vivo and in vitro.
|
53 |
31206670
|
Arf6 knockdown could cause ABCA1 recycling disorders, and thus, further aggravate cholesterol accumulation in podocytes under high-glucose (HG) conditions.
|
54 |
31206670
|
Our results demonstrate that HG-induced cholesterol accumulation and cellular injury in podocytes may be related to the recycling disorder of ABCA1 caused by the downexpression of Arf6 in DKD.
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55 |
32119711
|
This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes.
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56 |
32119711
|
Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP.
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57 |
32119711
|
The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor.
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58 |
32119711
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Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown.
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59 |
32119711
|
Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown.
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60 |
32119711
|
Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression.
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61 |
32119711
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Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP.
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62 |
32119711
|
We also provided evidence that Ang II activates Arf6 by degradation of CD2AP.
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63 |
32119711
|
This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes.
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64 |
32119711
|
Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP.
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65 |
32119711
|
The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor.
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66 |
32119711
|
Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown.
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67 |
32119711
|
Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown.
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68 |
32119711
|
Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression.
|
69 |
32119711
|
Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP.
|
70 |
32119711
|
We also provided evidence that Ang II activates Arf6 by degradation of CD2AP.
|
71 |
32119711
|
This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes.
|
72 |
32119711
|
Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP.
|
73 |
32119711
|
The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor.
|
74 |
32119711
|
Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown.
|
75 |
32119711
|
Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown.
|
76 |
32119711
|
Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression.
|
77 |
32119711
|
Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP.
|
78 |
32119711
|
We also provided evidence that Ang II activates Arf6 by degradation of CD2AP.
|
79 |
32119711
|
This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes.
|
80 |
32119711
|
Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP.
|
81 |
32119711
|
The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor.
|
82 |
32119711
|
Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown.
|
83 |
32119711
|
Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown.
|
84 |
32119711
|
Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression.
|
85 |
32119711
|
Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP.
|
86 |
32119711
|
We also provided evidence that Ang II activates Arf6 by degradation of CD2AP.
|
87 |
32119711
|
This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes.
|
88 |
32119711
|
Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP.
|
89 |
32119711
|
The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor.
|
90 |
32119711
|
Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown.
|
91 |
32119711
|
Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown.
|
92 |
32119711
|
Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression.
|
93 |
32119711
|
Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP.
|
94 |
32119711
|
We also provided evidence that Ang II activates Arf6 by degradation of CD2AP.
|