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PMID |
Sentence |
1 |
9916932
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WT1 and PAX-2 podocyte expression in Denys-Drash syndrome and isolated diffuse mesangial sclerosis.
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2 |
9916932
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One target gene of WT1 is PAX2, the expression of which is down-regulated in podocytes during early stages of nephrogenesis.
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3 |
9916932
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We demonstrate that WT1 mislocalization is associated with abnormal podocyte expression of PAX2 protein and RNA.
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4 |
9916932
|
We suggest that persistent expression of PAX2 is likely to result from the loss of WT1 dependent transcriptional repression and may participate in the pathological mechanisms leading to glomerular dysfunction.
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5 |
9916932
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Abnormal distribution of WT1 and PAX2 was also observed in isolated diffuse mesangial sclerosis suggesting that a defect in WT1 could also be operative in isolated diffuse mesangial sclerosis.
|
6 |
9916932
|
WT1 and PAX-2 podocyte expression in Denys-Drash syndrome and isolated diffuse mesangial sclerosis.
|
7 |
9916932
|
One target gene of WT1 is PAX2, the expression of which is down-regulated in podocytes during early stages of nephrogenesis.
|
8 |
9916932
|
We demonstrate that WT1 mislocalization is associated with abnormal podocyte expression of PAX2 protein and RNA.
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9 |
9916932
|
We suggest that persistent expression of PAX2 is likely to result from the loss of WT1 dependent transcriptional repression and may participate in the pathological mechanisms leading to glomerular dysfunction.
|
10 |
9916932
|
Abnormal distribution of WT1 and PAX2 was also observed in isolated diffuse mesangial sclerosis suggesting that a defect in WT1 could also be operative in isolated diffuse mesangial sclerosis.
|
11 |
9916932
|
WT1 and PAX-2 podocyte expression in Denys-Drash syndrome and isolated diffuse mesangial sclerosis.
|
12 |
9916932
|
One target gene of WT1 is PAX2, the expression of which is down-regulated in podocytes during early stages of nephrogenesis.
|
13 |
9916932
|
We demonstrate that WT1 mislocalization is associated with abnormal podocyte expression of PAX2 protein and RNA.
|
14 |
9916932
|
We suggest that persistent expression of PAX2 is likely to result from the loss of WT1 dependent transcriptional repression and may participate in the pathological mechanisms leading to glomerular dysfunction.
|
15 |
9916932
|
Abnormal distribution of WT1 and PAX2 was also observed in isolated diffuse mesangial sclerosis suggesting that a defect in WT1 could also be operative in isolated diffuse mesangial sclerosis.
|
16 |
9916932
|
WT1 and PAX-2 podocyte expression in Denys-Drash syndrome and isolated diffuse mesangial sclerosis.
|
17 |
9916932
|
One target gene of WT1 is PAX2, the expression of which is down-regulated in podocytes during early stages of nephrogenesis.
|
18 |
9916932
|
We demonstrate that WT1 mislocalization is associated with abnormal podocyte expression of PAX2 protein and RNA.
|
19 |
9916932
|
We suggest that persistent expression of PAX2 is likely to result from the loss of WT1 dependent transcriptional repression and may participate in the pathological mechanisms leading to glomerular dysfunction.
|
20 |
9916932
|
Abnormal distribution of WT1 and PAX2 was also observed in isolated diffuse mesangial sclerosis suggesting that a defect in WT1 could also be operative in isolated diffuse mesangial sclerosis.
|
21 |
9916932
|
WT1 and PAX-2 podocyte expression in Denys-Drash syndrome and isolated diffuse mesangial sclerosis.
|
22 |
9916932
|
One target gene of WT1 is PAX2, the expression of which is down-regulated in podocytes during early stages of nephrogenesis.
|
23 |
9916932
|
We demonstrate that WT1 mislocalization is associated with abnormal podocyte expression of PAX2 protein and RNA.
|
24 |
9916932
|
We suggest that persistent expression of PAX2 is likely to result from the loss of WT1 dependent transcriptional repression and may participate in the pathological mechanisms leading to glomerular dysfunction.
|
25 |
9916932
|
Abnormal distribution of WT1 and PAX2 was also observed in isolated diffuse mesangial sclerosis suggesting that a defect in WT1 could also be operative in isolated diffuse mesangial sclerosis.
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26 |
11877566
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WT1 and Pax2 are transcription factors involved in kidney development and phenotypic regulation of glomerular epithelial cells.
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27 |
11877566
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However, the role of WT1 and Pax2 in the development of CLs in primary FSGS is unclear.
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28 |
11877566
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Using immunohistochemistry, the expression of WT1, Pax2, and cytokeratin (CK), an epithelial marker never found in normal podocytes, was examined in 35 biopsy samples of primary FSGS.
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29 |
11877566
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Expression of WT1, Pax2, and CK was scantly positive in CSs.
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30 |
11877566
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WT1 and Pax2 are transcription factors involved in kidney development and phenotypic regulation of glomerular epithelial cells.
|
31 |
11877566
|
However, the role of WT1 and Pax2 in the development of CLs in primary FSGS is unclear.
|
32 |
11877566
|
Using immunohistochemistry, the expression of WT1, Pax2, and cytokeratin (CK), an epithelial marker never found in normal podocytes, was examined in 35 biopsy samples of primary FSGS.
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33 |
11877566
|
Expression of WT1, Pax2, and CK was scantly positive in CSs.
|
34 |
11877566
|
WT1 and Pax2 are transcription factors involved in kidney development and phenotypic regulation of glomerular epithelial cells.
|
35 |
11877566
|
However, the role of WT1 and Pax2 in the development of CLs in primary FSGS is unclear.
|
36 |
11877566
|
Using immunohistochemistry, the expression of WT1, Pax2, and cytokeratin (CK), an epithelial marker never found in normal podocytes, was examined in 35 biopsy samples of primary FSGS.
|
37 |
11877566
|
Expression of WT1, Pax2, and CK was scantly positive in CSs.
|
38 |
11877566
|
WT1 and Pax2 are transcription factors involved in kidney development and phenotypic regulation of glomerular epithelial cells.
|
39 |
11877566
|
However, the role of WT1 and Pax2 in the development of CLs in primary FSGS is unclear.
|
40 |
11877566
|
Using immunohistochemistry, the expression of WT1, Pax2, and cytokeratin (CK), an epithelial marker never found in normal podocytes, was examined in 35 biopsy samples of primary FSGS.
|
41 |
11877566
|
Expression of WT1, Pax2, and CK was scantly positive in CSs.
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42 |
12012385
|
These transcription factors include Pax2, WT1 (the Wilms tumor suppressor gene), Pod1 (capsulin, epicardin), Kreisler (maf-1), lmx1b, and mf2.
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43 |
12386275
|
WT1 and Pax2 are transcription factors involved in kidney development and phenotypic regulation of glomerular epithelial cells.
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44 |
12386275
|
To investigate the contribution of WT1 and Pax2 to the development of the CL in primary FSGS, immunohistological studies were performed using renal biopsy specimens on the expression of WT1, Pax2 and cytokeratin (CK), which is an epithelial marker but never found in normal podocytes.
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45 |
12386275
|
WT1 and Pax2 are transcription factors involved in kidney development and phenotypic regulation of glomerular epithelial cells.
|
46 |
12386275
|
To investigate the contribution of WT1 and Pax2 to the development of the CL in primary FSGS, immunohistological studies were performed using renal biopsy specimens on the expression of WT1, Pax2 and cytokeratin (CK), which is an epithelial marker but never found in normal podocytes.
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47 |
12488983
|
Recently, abnormal expression of WT1 and PAX2 was shown in the podocytes in diffuse mesangial sclerosis (DMS) associated with DDS and isolated DMS.
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48 |
12488983
|
Immunohistochemical analysis of WT1, PAX2, vimentin, cytokeratin, and epithelial membrane antigen was performed in the kidney specimens obtained at autopsy or surgery.
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49 |
12488983
|
Abnormal expression of WT1 and PAX2 in the EHBCE was observed in both patients, supporting our hypothesis.
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50 |
12488983
|
Recently, abnormal expression of WT1 and PAX2 was shown in the podocytes in diffuse mesangial sclerosis (DMS) associated with DDS and isolated DMS.
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51 |
12488983
|
Immunohistochemical analysis of WT1, PAX2, vimentin, cytokeratin, and epithelial membrane antigen was performed in the kidney specimens obtained at autopsy or surgery.
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52 |
12488983
|
Abnormal expression of WT1 and PAX2 in the EHBCE was observed in both patients, supporting our hypothesis.
|
53 |
12488983
|
Recently, abnormal expression of WT1 and PAX2 was shown in the podocytes in diffuse mesangial sclerosis (DMS) associated with DDS and isolated DMS.
|
54 |
12488983
|
Immunohistochemical analysis of WT1, PAX2, vimentin, cytokeratin, and epithelial membrane antigen was performed in the kidney specimens obtained at autopsy or surgery.
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55 |
12488983
|
Abnormal expression of WT1 and PAX2 in the EHBCE was observed in both patients, supporting our hypothesis.
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56 |
15505531
|
The glomerular basement membrane is composed of a multitude of proteins, including collagen IV, heparan sulfate proteoglycans, and laminin, among others.
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57 |
15505531
|
The exact mechanism by which nephrin controls permselectivity is not yet clear, but it is known to interact with several podocyte proteins including CD2AP, podocin, and alpha-actinin-4.
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58 |
15505531
|
A host of transcription factors, especially WT1 and PAX2, play a significant role in modulating podocyte function.
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59 |
16761013
|
We used Synaptopodin, vascular endothelial growth factor, and CD10 as podocyte markers, CK8 and PAX2 as PEC markers and Ki-67 as marker of cell proliferation.
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60 |
16761013
|
The proliferating PAX-2 and CK8 positive cells that covered the capillary tuft were always in continuity with PAX-2/CK8 positive cells lining Bowman's capsule.
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61 |
16761013
|
We used Synaptopodin, vascular endothelial growth factor, and CD10 as podocyte markers, CK8 and PAX2 as PEC markers and Ki-67 as marker of cell proliferation.
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62 |
16761013
|
The proliferating PAX-2 and CK8 positive cells that covered the capillary tuft were always in continuity with PAX-2/CK8 positive cells lining Bowman's capsule.
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63 |
16943305
|
The expression of podocyte-specific proteins (podocalyxin, glomerular epithelial protein-1, podocin, nephrin, synaptopodin, and alpha-actinin-4), podocyte synthesized proteins (vascular endothelial growth factor and novH), transcription factors (WT1 and PAX2), cyclin-dependent kinase inhibitor p57, and intermediate filaments (cytokeratins and vimentin) was tested.
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64 |
16943305
|
WT1 and p57 were expressed in some parietal cells, whereas PAX2 was present in all or most of them, so some parietal cells coexpressed WT1 and PAX2.
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65 |
16943305
|
The expression of podocyte-specific proteins (podocalyxin, glomerular epithelial protein-1, podocin, nephrin, synaptopodin, and alpha-actinin-4), podocyte synthesized proteins (vascular endothelial growth factor and novH), transcription factors (WT1 and PAX2), cyclin-dependent kinase inhibitor p57, and intermediate filaments (cytokeratins and vimentin) was tested.
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66 |
16943305
|
WT1 and p57 were expressed in some parietal cells, whereas PAX2 was present in all or most of them, so some parietal cells coexpressed WT1 and PAX2.
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67 |
17466922
|
In this review, the role of Wilms tumor 1 (WT1), LIM homeobox transcription factor 1, beta (Lmx1b), pod1, pax-2, kreisler, nuclear factor-kappa B (NF-kappaB), smad7, and zinc fingers and homeoboxes (ZHX) proteins in the development of podocyte disease is outlined.
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68 |
19390481
|
At birth, the lambs were killed, and their kidneys were removed to study the changes in histology, podocytes, and expression of paired-box 2 (PAX2) and VEGF.
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69 |
19579288
|
We found that human glomeruli deprived of the Bowman's capsule contain a population of CD133+CD146+ cells and a population of CD133-CD146+ cells expressing mesenchymal stem cell (MSC) markers and renal stem cell markers CD24 and Pax-2.
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70 |
19579288
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The CD133+CD146+ cells differed from those previously isolated from Bowman's capsule as they co-expressed endothelial markers, such as CD31 and von Willebrand factor (vWF), were CD24-negative and were not clonogenic, suggesting an endothelial commitment.
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71 |
19579288
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In addition to osteogenic, adipogenic, and chondrogenic differentiation, these cells were able to differentiate to endothelial cells and epithelial cells expressing podocytes markers such as nephrin, podocin, and synaptopodin.
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72 |
19579288
|
Moreover, Gl-MSC when cultured in appropriate conditions, acquired mesangial cell markers such as alpha-smooth muscle actin (alpha-SMA) and angiotensin II (AT-II) receptor I.
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73 |
20818613
|
To identify morphological and developmental changes in protein and RNA expression patterns during nephrogenesis, immunohistochemistry and quantitative real-time PCR were used to assess temporal and spatial expression of WT1, Pax2, Nestin, Synaptopodin, alpha-smooth muscle actin (α-SMA), CD31, vascular endothelial growth factor (VEGF), and Gremlin.
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74 |
20818613
|
Mature podocytes expressing WT1, Nestin, and Synaptopodin were observed from the mid-third trimester through adulthood.
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75 |
20818613
|
The developing glomerulus was positive for α-SMA (vascular smooth muscle) and Gremlin (mesangial cells), CD31 (glomerular endothelium), and VEGF (endothelium), and showed loss of expression of these markers as glomerular maturation was completed.
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76 |
21160460
|
There was focal loss of the podocyte markers synaptopodin, glomerular epithelial protein 1 (GLEPP-1), nephrin, and vascular endothelial growth factor (VEGF), particularly at sites of capsular adhesions in otherwise histologically normal glomeruli.
|
77 |
21160460
|
Cells displaying the parietal epithelial cell markers PAX2 (paired box gene 2) and the cytokeratins were also positive for the proliferating cell marker, proliferating cell nuclear antigen.
|
78 |
22129965
|
Single and double immunostaining were performed with antibodies to the PEC protein paired box gene 2 (PAX2) and tight junction protein claudin-1, the podocyte-specific protein Wilms' tumor 1 (WT-1), and the proliferating cell protein (Ki-67).
|
79 |
22129965
|
The increase in PEC number was due to proliferation (increase in PAX2/Ki-67 double-positive cells).
|
80 |
22129965
|
Aging was accompanied by a progressive increase in the number of glomerular cells double staining for PAX2 and WT-1.
|
81 |
22129965
|
Single and double immunostaining were performed with antibodies to the PEC protein paired box gene 2 (PAX2) and tight junction protein claudin-1, the podocyte-specific protein Wilms' tumor 1 (WT-1), and the proliferating cell protein (Ki-67).
|
82 |
22129965
|
The increase in PEC number was due to proliferation (increase in PAX2/Ki-67 double-positive cells).
|
83 |
22129965
|
Aging was accompanied by a progressive increase in the number of glomerular cells double staining for PAX2 and WT-1.
|
84 |
22129965
|
Single and double immunostaining were performed with antibodies to the PEC protein paired box gene 2 (PAX2) and tight junction protein claudin-1, the podocyte-specific protein Wilms' tumor 1 (WT-1), and the proliferating cell protein (Ki-67).
|
85 |
22129965
|
The increase in PEC number was due to proliferation (increase in PAX2/Ki-67 double-positive cells).
|
86 |
22129965
|
Aging was accompanied by a progressive increase in the number of glomerular cells double staining for PAX2 and WT-1.
|
87 |
22529955
|
In the very early phases of primary culture, rapid changes in gene expression (e.g. of WT-1 and Pax-2) were observed.
|
88 |
22529955
|
Of the classical markers, synaptopodin and podoplanin expression were differentially regulated the most in primary PEC and podocyte cultures.
|
89 |
22610571
|
We recently found that human glomeruli deprived of the Bowman's capsule contain a population of CD133(-)CD146(+) cells that coexpress the typical mesenchymal stem cells (MSCs) markers (such as CD29, CD105, and CD73) and renal specific stem cell markers (such us CD24 and Pax2).
|
90 |
22677342
|
The renal protein expression of renin and angiotensin II was reduced at birth day and increased at weaning.
|
91 |
22677342
|
Maternal DEHP exposure also led to reduced mRNA expression of some renal development involved genes at birth day, including Foxd1, Gdnf, Pax2 and Wnt11.
|
92 |
22677342
|
While, the mRNA expression of some genes was raised, including Bmp4, Cdh11, Calm1 and Ywhab.
|
93 |
23769837
|
A subset of cells lining Bowman's capsule activated expression of the glomerular parietal epithelial cell markers paired box protein PAX2 and claudin-1.
|
94 |
23769837
|
A subset of labeled cells within the glomerular tuft expressed the podocyte markers Wilms tumor protein 1, nephrin, podocin, and synaptopodin.
|
95 |
24154691
|
Using a podocyte-specific injury model of FSGS carrying a genetic podocyte tag combined with double immunostaining by different sets of podocytes and parietal epithelial cell (PEC) markers [nestin/Pax8, Wilms' tumor-1 (WT1)/claudin1, and podocalyxin/Pax2], we investigated the direction of epithelial phenotypic transition and its role in FSGS.
|
96 |
24154691
|
In addition, the average numbers of double-positive cells for X-gal/Pax8, nestin/Pax8 and podocalyxin/Pax2 staining in the FSGS mice were comparable, whereas those of WT1/claudin1 were significantly increased.
|
97 |
24676634
|
As predicted by in silico structural modeling analyses, in vitro functional studies documented that several of the FSGS-associated PAX2 mutations perturb protein function by affecting proper binding to DNA and transactivation activity or by altering the interaction of PAX2 with repressor proteins, resulting in enhanced repressor activity.
|
98 |
25460740
|
Moreover, the effects of the HO-system on podocyte cytoskeletal proteins like podocin, podocalyxin, CD2-associated-protein (CD2AP) and proteins of regeneration/repair like beta-catenin, Oct3/4, WT1 and Pax2 in renal tissue from normoglycemic obese Zucker-fatty rats (ZFs) have not been reported.
|
99 |
25460740
|
These were associated with enhanced expression of beta-catenin, Oct3/4, WT1, Pax2 and nephrin, an essential transmembrane protein required for the formation of the scaffoldings of the podocyte slit-diaphragm, permitting the filtration of small ions, but not massive excretion of proteins, hence proteinuria.
|
100 |
25460740
|
Besides nephrin, hemin also enhanced other important podocyte-regulators including, podocalyxin, podocin and CD2AP.
|
101 |
25460740
|
Collectively, these data suggest that hemin ameliorates nephropathy by potentiating the expression of proteins of repair/regeneration, abating oxidative/inflammatory mediators, reducing renal histo-pathological lesions, while enhancing nephrin, podocin, podocalyxin, CD2AP and creatinine clearance, with corresponding reduction of albuminuria/proteinuria suggesting improved renal function in hemin-treated ZFs.
|
102 |
25460740
|
Moreover, the effects of the HO-system on podocyte cytoskeletal proteins like podocin, podocalyxin, CD2-associated-protein (CD2AP) and proteins of regeneration/repair like beta-catenin, Oct3/4, WT1 and Pax2 in renal tissue from normoglycemic obese Zucker-fatty rats (ZFs) have not been reported.
|
103 |
25460740
|
These were associated with enhanced expression of beta-catenin, Oct3/4, WT1, Pax2 and nephrin, an essential transmembrane protein required for the formation of the scaffoldings of the podocyte slit-diaphragm, permitting the filtration of small ions, but not massive excretion of proteins, hence proteinuria.
|
104 |
25460740
|
Besides nephrin, hemin also enhanced other important podocyte-regulators including, podocalyxin, podocin and CD2AP.
|
105 |
25460740
|
Collectively, these data suggest that hemin ameliorates nephropathy by potentiating the expression of proteins of repair/regeneration, abating oxidative/inflammatory mediators, reducing renal histo-pathological lesions, while enhancing nephrin, podocin, podocalyxin, CD2AP and creatinine clearance, with corresponding reduction of albuminuria/proteinuria suggesting improved renal function in hemin-treated ZFs.
|
106 |
26154924
|
WT1 controls metanephric mesenchyme (MM) self-renewal and proliferation mainly by regulating FGF and BMP-pSMAD signaling pathways as well as Sall1 and Pax2, encoding key transcription factors; WT1 drives MM differentiation and mesenchyme-epithelial transition by targeting Fgf8 and Wnt4; WT1 defines podocyte identity by activation of other podocyte-specific transcription factors, including Mafb, Lmx1b, FoxC2, and Tcf21.
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107 |
26458176
|
By recapitulating metanephric kidney development in vitro, we generate SIX2+ SALL1+ WT1+ PAX2+ NPCs with 90% efficiency within 9 days of differentiation.
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108 |
27588086
|
In addition, the expression of octamer-binding transcription factor 4 (Oct-4), a stem cell marker, was detected and suggested that kidney-specific stem cells were present in the DT-treated tissue samples.
|
109 |
27588086
|
The unique cells were positive for Oct-4 and Pax-2; thus suggesting that the identified cells were kidney-derived stem cells.
|
110 |
28852936
|
Subsequently, thus-obtained Osr1+ cells were induced further with activin-A (10 ng/ml), RA (10 ng/ml), BMP-7 (2.5 ng/ml), EGF (30 ng/ml) and bFGF (30 ng/ml) for 9 days.
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111 |
28852936
|
Consequently, differentiated cells were immunopositive for anti-podocin, anti-synaptopodin and anti-GLEPP1 monoclonal antibodies.
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112 |
28852936
|
These cells showed expression of early podocyte markers PAX2 and Wt1 at day 3 followed by day 6 and mature podocyte markers NPHS1, SULT1B1, NPHS2 and Synaptopodin at day 9.
|
113 |
29307170
|
Immunohistochemical staining for PAX-2, Ki-67, and synaptopodin was performed to evaluate cell proliferation in the kidney tissues.Results: After 4 weeks of treatment, islet transplantation significantly alleviated damage to the podocytes and increased the number of glomerular transition cells compared to the DN and IN groups, which were defined as cells that double-stained for PAX-2 and synaptopodin in membranous nephropathy.
|
114 |
29357419
|
Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu.
|
115 |
29357419
|
HG-induced DPD dedifferentiation manifested in the form of downregulation of Wilms' tumor 1 (WT1) and upregulation of paired box 2 (PAX2) expression.
|
116 |
29357419
|
WT1-silenced DPDs displayed enhanced expression of PAX2.
|
117 |
29357419
|
Immunoprecipitation of DPD cellular lysates with anti-WT1 antibody revealed formation of WT1 repressor complexes containing Polycomb group proteins, enhancer of zeste homolog 2, menin, and DNA methyltransferase (DNMT1), whereas silencing of either WT1 or DNMT1 disrupted this complex with enhanced expression of PAX2.
|
118 |
29357419
|
HG downregulated DPD expression of APOL1. miR193a-overexpressing DPDs displayed downregulation of APOL1 and enhanced expression of dedifferentiating markers; conversely, silencing of miR193a enhanced the expression of APOL1 and preserved DPD phenotype.
|
119 |
29357419
|
Moreover, stably APOL1G0-overexpressing DPDs displayed the enhanced expression of WT1 but attenuated expression of miR193a; nonetheless, silencing of APOL1 reversed these effects.
|
120 |
29357419
|
Vitamin D receptor agonist downregulated miR193a, upregulated APOL1 expression, and prevented dedifferentiation of DPDs in HG milieu.
|
121 |
29357419
|
Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu.
|
122 |
29357419
|
HG-induced DPD dedifferentiation manifested in the form of downregulation of Wilms' tumor 1 (WT1) and upregulation of paired box 2 (PAX2) expression.
|
123 |
29357419
|
WT1-silenced DPDs displayed enhanced expression of PAX2.
|
124 |
29357419
|
Immunoprecipitation of DPD cellular lysates with anti-WT1 antibody revealed formation of WT1 repressor complexes containing Polycomb group proteins, enhancer of zeste homolog 2, menin, and DNA methyltransferase (DNMT1), whereas silencing of either WT1 or DNMT1 disrupted this complex with enhanced expression of PAX2.
|
125 |
29357419
|
HG downregulated DPD expression of APOL1. miR193a-overexpressing DPDs displayed downregulation of APOL1 and enhanced expression of dedifferentiating markers; conversely, silencing of miR193a enhanced the expression of APOL1 and preserved DPD phenotype.
|
126 |
29357419
|
Moreover, stably APOL1G0-overexpressing DPDs displayed the enhanced expression of WT1 but attenuated expression of miR193a; nonetheless, silencing of APOL1 reversed these effects.
|
127 |
29357419
|
Vitamin D receptor agonist downregulated miR193a, upregulated APOL1 expression, and prevented dedifferentiation of DPDs in HG milieu.
|
128 |
29357419
|
Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu.
|
129 |
29357419
|
HG-induced DPD dedifferentiation manifested in the form of downregulation of Wilms' tumor 1 (WT1) and upregulation of paired box 2 (PAX2) expression.
|
130 |
29357419
|
WT1-silenced DPDs displayed enhanced expression of PAX2.
|
131 |
29357419
|
Immunoprecipitation of DPD cellular lysates with anti-WT1 antibody revealed formation of WT1 repressor complexes containing Polycomb group proteins, enhancer of zeste homolog 2, menin, and DNA methyltransferase (DNMT1), whereas silencing of either WT1 or DNMT1 disrupted this complex with enhanced expression of PAX2.
|
132 |
29357419
|
HG downregulated DPD expression of APOL1. miR193a-overexpressing DPDs displayed downregulation of APOL1 and enhanced expression of dedifferentiating markers; conversely, silencing of miR193a enhanced the expression of APOL1 and preserved DPD phenotype.
|
133 |
29357419
|
Moreover, stably APOL1G0-overexpressing DPDs displayed the enhanced expression of WT1 but attenuated expression of miR193a; nonetheless, silencing of APOL1 reversed these effects.
|
134 |
29357419
|
Vitamin D receptor agonist downregulated miR193a, upregulated APOL1 expression, and prevented dedifferentiation of DPDs in HG milieu.
|
135 |
34411489
|
miR-193a as a potential mediator of WT-1/synaptopodin in the renoprotective effect of Losartan on diabetic kidney.
|
136 |
34411489
|
Next, immunohistochemistry and immunofluorescence were used to detect Wilms tumor protein 1 (WT-1) and synaptopodin expression, respectively.
|
137 |
34411489
|
Protein levels of WT-1, synaptopodin, claudin1, and Pax-2 were assessed by Western blotting and real-time PCR.
|
138 |
34411489
|
In addition, Losartan significantly upregulated the immunopositive cell numbers of WT-1, the expression of WT-1 and synaptopodin in renal tissue.
|
139 |
34411489
|
By contrast, expression of claudin1 and Pax-2 in renal tissue were decreased in db/db-losartan group.
|
140 |
34411489
|
miR-193a as a potential mediator of WT-1/synaptopodin in the renoprotective effect of Losartan on diabetic kidney.
|
141 |
34411489
|
Next, immunohistochemistry and immunofluorescence were used to detect Wilms tumor protein 1 (WT-1) and synaptopodin expression, respectively.
|
142 |
34411489
|
Protein levels of WT-1, synaptopodin, claudin1, and Pax-2 were assessed by Western blotting and real-time PCR.
|
143 |
34411489
|
In addition, Losartan significantly upregulated the immunopositive cell numbers of WT-1, the expression of WT-1 and synaptopodin in renal tissue.
|
144 |
34411489
|
By contrast, expression of claudin1 and Pax-2 in renal tissue were decreased in db/db-losartan group.
|