# |
PMID |
Sentence |
1 |
18245810
|
The small GTPase RhoA is activated by the angiotensin II (AngII) type 1 receptor (AT1R), which is part of the local renin-angiotensin system that is involved in podocyte injury preceding glomerular crescent formation.
|
2 |
18245810
|
We demonstrated previously that inhibition of AT1R protects against crescentic glomerular injury in Fc receptor-deficient mice (gamma -/-) with anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM GN).
|
3 |
18245810
|
Fasudil markedly attenuated crescentic GN with a significant decrease in proteinuria and hematuria, infiltration of T cells and monocytes/macrophages as well as their local proliferation, and preservation of podocyte-specific proteins, including WT-1 and nephrin, in glomeruli.
|
4 |
18245810
|
In vitro studies showed that AngII induced the down-regulation of both nephrin and WT-1 expression in podocytes, which was reversed by fasudil in a dose-dependent manner.
|
5 |
19661163
|
Renal FcRn reclaims albumin but facilitates elimination of IgG.
|
6 |
19661163
|
The widely distributed neonatal Fc receptor (FcRn) contributes to maintaining serum levels of albumin and IgG in adults.
|
7 |
19661163
|
Here, we evaluated the role of renal FcRn in albumin and IgG metabolism.
|
8 |
19661163
|
Compared with wild-type controls, FcRn(-/-) mice had a lower t((1/2)) for albumin (28.7 versus 39.9 h) and IgG (29.5 versus 66.1 h).
|
9 |
19661163
|
Renal loss of albumin could account for the former, suggested by the progressive development of hypoalbuminemia in wild-type mice transplanted with FcRn-deficient kidneys.
|
10 |
19661163
|
Furthermore, serum albumin levels returned to normal in FcRn(-/-) recipients of wild-type kidneys after removing the native FcRn-deficient kidneys.
|
11 |
19661163
|
Taken together, these data suggest that renal FcRn reclaims albumin, thereby maintaining the serum concentration of albumin, but facilitates the loss of IgG from plasma protein pools.
|
12 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
13 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
14 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
15 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
16 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
17 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
18 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
19 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
20 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
21 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
22 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
23 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
24 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
25 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
26 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
27 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
28 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
29 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
30 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
31 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
32 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
33 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
34 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
35 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
36 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
37 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
38 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
39 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
40 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
41 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
42 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
43 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
44 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
45 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
46 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
47 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
48 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
49 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
50 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
51 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
52 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
53 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
54 |
22406365
|
Neonatal Fc receptor stimulation induces ubiquitin c-terminal hydrolase-1 overexpression in podocytes through activation of p38 mitogen-activated protein kinase.
|
55 |
22406365
|
Neonatal Fc receptor is newly recognized to be present on human renal podocytes.
|
56 |
22406365
|
It is presumed that neonatal Fc receptor serves as a sensor for immune stimulation transduction and is involved in the pathogenesis of podocyte injury.
|
57 |
22406365
|
In our current study, we found that neonatal Fc receptor was constitutively expressed in normal podocytes and up-regulated by immune stimulation induced by antithymocyte serum.
|
58 |
22406365
|
An increase in neonatal Fc receptor expression was observed in human podocytes within diseased glomeruli in 97 cases of various glomerulonephritides.
|
59 |
22406365
|
Further study showed that neonatal Fc receptor up-regulated the expression of ubiquitin c-terminal hydrolase-1 via activation of p38 in podocytes subjected to immune stimulation in vitro.
|
60 |
22406365
|
These data suggest that neonatal Fc receptor acts as an immune sensor that evokes an inflammatory response, which may lead to functional and morphological changes in podocytes in glomerulonephritides.
|
61 |
23970123
|
Genetic deletion of the neonatal Fc receptor (FcRn), which rescues albumin and IgG from lysosomal degradation, abolished transcytosis of both types of transgenic albumin and IgG in proximal tubular cells.
|
62 |
24126590
|
In a recent study using transgenic mice with inducible podocyte-specific expression of tagged albumin, Tenten and colleagues report transtubular transport of albumin, possibly mediated by the neonatal Fc receptor.
|
63 |
24357670
|
Neonatal Fc receptor promotes immune complex-mediated glomerular disease.
|
64 |
24357670
|
The neonatal Fc receptor (FcRn) is a major regulator of IgG and albumin homeostasis systemically and in the kidneys.
|
65 |
24357670
|
Neonatal Fc receptor promotes immune complex-mediated glomerular disease.
|
66 |
24357670
|
The neonatal Fc receptor (FcRn) is a major regulator of IgG and albumin homeostasis systemically and in the kidneys.
|
67 |
24573386
|
Once internalized, FITC-albumin colocalized with EEA1 and LAMP1, endocytic markers, and with the neonatal Fc receptor, a marker for transcytosis.
|
68 |
27682967
|
We suggest that a specific anti-EBNA1 antibody internalized in the podocytes via the neonatal Fc receptor might cross-react with a major protein present in the same cell trafficking compartment.
|
69 |
28259932
|
Albumin-based nanoparticles as methylprednisolone carriers for targeted delivery towards the neonatal Fc receptor in glomerular podocytes.
|
70 |
28259932
|
The present study aimed to selectively deliver albumin‑methylprednisolone (MP) nanoparticles towards glomerular podocytes, which highly express the specific neonatal Fc receptor (FcRn) of albumin.
|
71 |
28259932
|
Albumin-based nanoparticles as methylprednisolone carriers for targeted delivery towards the neonatal Fc receptor in glomerular podocytes.
|
72 |
28259932
|
The present study aimed to selectively deliver albumin‑methylprednisolone (MP) nanoparticles towards glomerular podocytes, which highly express the specific neonatal Fc receptor (FcRn) of albumin.
|
73 |
30811433
|
Differential trafficking of albumin and IgG facilitated by the neonatal Fc receptor in podocytes in vitro and in vivo.
|
74 |
30811433
|
In other epithelial cells, the neonatal Fc receptor (FcRn) is required to salvage albumin and IgG from the degradative pathway thereby allowing these proteins to be transcytosed or recycled.
|
75 |
30811433
|
Here we directly examine the role of FcRn in albumin and IgG trafficking in podocytes by studying handling of these proteins in FcRn knockout (KO) podocytes in vitro and in a podocyte-specific FcRn knockout mice in vivo.
|
76 |
30811433
|
In vitro, we find that knockout of FcRn leads to IgG accumulation in podocytes but does not alter albumin trafficking.
|
77 |
30811433
|
Similarly, in vivo, podocyte-specific knockout of FcRn does not result in albumin accumulation in podocytes in vivo as measured by mean albumin fluorescence intensity whereas these mice demonstrate significant intraglomerular accumulation of IgG over time.
|
78 |
30811433
|
In addition we find that podocyte-specific FcRn KO mice demonstrate mesangial expansion as they age and activation of mesangial cells as demonstrated by increased expression of α-smooth muscle actin.
|
79 |
30811433
|
Differential trafficking of albumin and IgG facilitated by the neonatal Fc receptor in podocytes in vitro and in vivo.
|
80 |
30811433
|
In other epithelial cells, the neonatal Fc receptor (FcRn) is required to salvage albumin and IgG from the degradative pathway thereby allowing these proteins to be transcytosed or recycled.
|
81 |
30811433
|
Here we directly examine the role of FcRn in albumin and IgG trafficking in podocytes by studying handling of these proteins in FcRn knockout (KO) podocytes in vitro and in a podocyte-specific FcRn knockout mice in vivo.
|
82 |
30811433
|
In vitro, we find that knockout of FcRn leads to IgG accumulation in podocytes but does not alter albumin trafficking.
|
83 |
30811433
|
Similarly, in vivo, podocyte-specific knockout of FcRn does not result in albumin accumulation in podocytes in vivo as measured by mean albumin fluorescence intensity whereas these mice demonstrate significant intraglomerular accumulation of IgG over time.
|
84 |
30811433
|
In addition we find that podocyte-specific FcRn KO mice demonstrate mesangial expansion as they age and activation of mesangial cells as demonstrated by increased expression of α-smooth muscle actin.
|
85 |
30903736
|
The neonatal Fc receptor: Key to homeostasic control of IgG and IgG-related biopharmaceuticals.
|
86 |
30903736
|
These properties are due to a unique receptor, the neonatal Fc receptor (FcRn).
|
87 |
30903736
|
Although FcRn is named for its function of transferring IgG across the placenta from maternal to fetal circulation, FcRn functions throughout life to maintain IgG and albumin concentrations.
|
88 |
30903736
|
FcRn protects IgG and albumin from intracellular degradation and recycles them back into the circulation.
|
89 |
30903736
|
The neonatal Fc receptor: Key to homeostasic control of IgG and IgG-related biopharmaceuticals.
|
90 |
30903736
|
These properties are due to a unique receptor, the neonatal Fc receptor (FcRn).
|
91 |
30903736
|
Although FcRn is named for its function of transferring IgG across the placenta from maternal to fetal circulation, FcRn functions throughout life to maintain IgG and albumin concentrations.
|
92 |
30903736
|
FcRn protects IgG and albumin from intracellular degradation and recycles them back into the circulation.
|
93 |
31553647
|
Knockout of the neonatal Fc receptor in cultured podocytes alters IL-6 signaling and the actin cytoskeleton.
|
94 |
31553647
|
The neonatal Fc receptor (FcRn) has been shown to be required for antigen presentation in dendritic cells, and global knockout of FcRn attenuates immune-mediated kidney disease.
|
95 |
31553647
|
Here we examined the role of FcRn in the IL-6-mediated inflammatory response in podocytes.
|
96 |
31553647
|
We examined IL-6 production by ELISA and expression by qPCR in wild type (WT) and FcRn knockout (KO) podocytes after treatment with proinflammatory stimuli as well as IL-6-mediated signaling via the JAK/STAT pathway.
|
97 |
31553647
|
We found that FcRn KO podocytes produced minimal amount of IL-6 after treatment with albumin, IgG, or immune complexes whereas WT podocytes had a robust response.
|
98 |
31553647
|
FcRn KO podocytes also had minimal expression of IL-6 compared with WT.
|
99 |
31553647
|
Cultured FcRn KO podocytes also demonstrated abnormal stress fibers compared with WT and the defect could be rescued by IL-6 treatment.
|
100 |
31553647
|
This study shows that in podocytes, FcRn modulates the IL-6 mediated response to proinflammatory stimuli and regulates podocytes actin structure, motility and synaptopodin expression.
|
101 |
31553647
|
Knockout of the neonatal Fc receptor in cultured podocytes alters IL-6 signaling and the actin cytoskeleton.
|
102 |
31553647
|
The neonatal Fc receptor (FcRn) has been shown to be required for antigen presentation in dendritic cells, and global knockout of FcRn attenuates immune-mediated kidney disease.
|
103 |
31553647
|
Here we examined the role of FcRn in the IL-6-mediated inflammatory response in podocytes.
|
104 |
31553647
|
We examined IL-6 production by ELISA and expression by qPCR in wild type (WT) and FcRn knockout (KO) podocytes after treatment with proinflammatory stimuli as well as IL-6-mediated signaling via the JAK/STAT pathway.
|
105 |
31553647
|
We found that FcRn KO podocytes produced minimal amount of IL-6 after treatment with albumin, IgG, or immune complexes whereas WT podocytes had a robust response.
|
106 |
31553647
|
FcRn KO podocytes also had minimal expression of IL-6 compared with WT.
|
107 |
31553647
|
Cultured FcRn KO podocytes also demonstrated abnormal stress fibers compared with WT and the defect could be rescued by IL-6 treatment.
|
108 |
31553647
|
This study shows that in podocytes, FcRn modulates the IL-6 mediated response to proinflammatory stimuli and regulates podocytes actin structure, motility and synaptopodin expression.
|
109 |
32531122
|
Mechanistically, we found that CAMK4 phosphorylates GSK3β (glycogen synthase kinase 3 beta), activates the Wnt pathway and stabilizes the nephrin transcriptional repressor SNAIL.
|
110 |
32531122
|
Silencing neonatal Fc Receptor (FcRn) or CAMK4 prevented the podocyte-damaging effects of IgG from patients with TG.
|
111 |
33370294
|
Podocyte-specific knockout of the neonatal Fc receptor (FcRn) results in differential protection depending on the model of glomerulonephritis.
|
112 |
33370294
|
In traditional APCs, the neonatal Fc receptor (FcRn) is required for antigen presentation and global knockout of FcRn protects against glomerulonephritis.
|
113 |
33370294
|
Interferon gamma (IFNγ) induced MHCII expression in both WT and KO podocytes but did not change CD80 expression.
|
114 |
33370294
|
Neither WT nor KO expressed CD86 or inducible costimulatory ligand (ICOSL) at baseline or with IFNγ.
|
115 |
33370294
|
Podocyte-specific knockout of the neonatal Fc receptor (FcRn) results in differential protection depending on the model of glomerulonephritis.
|
116 |
33370294
|
In traditional APCs, the neonatal Fc receptor (FcRn) is required for antigen presentation and global knockout of FcRn protects against glomerulonephritis.
|
117 |
33370294
|
Interferon gamma (IFNγ) induced MHCII expression in both WT and KO podocytes but did not change CD80 expression.
|
118 |
33370294
|
Neither WT nor KO expressed CD86 or inducible costimulatory ligand (ICOSL) at baseline or with IFNγ.
|
119 |
33606211
|
In other epithelial cells including renal proximal tubular cells, the neonatal Fc receptor (FcRn) is required to divert albumin and IgG from the degradative pathway which allows these proteins to be recycled or transcytosed.
|
120 |
33606211
|
To examine the role of podocyte FcRn in albumin and IgG trafficking in vivo, we detail the creation of a podocyte-specific FcRn knockout mouse and describe methods for examining intraglomerular detection of albumin and IgG in these mice.
|
121 |
34071680
|
Long-lasting investigation in this area has delineated the principal route of its catabolism involving glomerular filtration, tubular endocytic uptake via the multiligand scavenger receptor tandem-megalin and cubilin-amnionless complex, as well as lysosomal degradation to amino acids.
|
122 |
34071680
|
Direct uptake of albumin in glomerular podocytes via receptor for crystallizable region of immunoglobulins (neonatal FC receptor) was demonstrated.
|
123 |
34450430
|
In Western blot and immunofluorescence analysis in vitro, methyl-beta-cyclodextrin (MBCD) treatment significantly decreased the expression of caveolin-1 and albumin in cultured human podocytes after incubation with albumin; additionally, MBCD interfered with albumin endocytosis through caveolae in the experiment using Transwell plates.
|
124 |
34450430
|
In the immunofluorescence analysis, albumin was incubated with cultured human podocytes, and colocalisation analysis with organelles and cytoskeletons in the podocytes showed that albumin particles colocalised with caveolin-1 and Fc-receptor but not clathrin in endocytosis, colocalised with actin cytoskeleton but not microtubules in transcytosis, and colocalised with early endosomes and lysosomes but not proteasome, endoplasmic reticulum, or Golgi apparatus.
|
125 |
34450430
|
Albumin enters through caveolae with the Fc-receptor, moves along actin, and reaches the early endosome, where some of them are sorted for lysosomal degradation, and others are directly transported outside the cells through exocytosis.
|
126 |
34450430
|
In Western blot and immunofluorescence analysis in vitro, methyl-beta-cyclodextrin (MBCD) treatment significantly decreased the expression of caveolin-1 and albumin in cultured human podocytes after incubation with albumin; additionally, MBCD interfered with albumin endocytosis through caveolae in the experiment using Transwell plates.
|
127 |
34450430
|
In the immunofluorescence analysis, albumin was incubated with cultured human podocytes, and colocalisation analysis with organelles and cytoskeletons in the podocytes showed that albumin particles colocalised with caveolin-1 and Fc-receptor but not clathrin in endocytosis, colocalised with actin cytoskeleton but not microtubules in transcytosis, and colocalised with early endosomes and lysosomes but not proteasome, endoplasmic reticulum, or Golgi apparatus.
|
128 |
34450430
|
Albumin enters through caveolae with the Fc-receptor, moves along actin, and reaches the early endosome, where some of them are sorted for lysosomal degradation, and others are directly transported outside the cells through exocytosis.
|