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PMID |
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1 |
34857869
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Co-cultured using a magnetic spheroid formation approach, conditionally immortalised (CI) human podocytes and glomerular endothelial cells (GEnCs) deposited mature, organized isoforms of collagen IV and Laminin.
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2 |
34857869
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We demonstrate a dramatic upregulation of key podocyte (podocin, nephrin and podocalyxin) and GEnC (pecam-1) markers.
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3 |
31853790
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The mechanisms underlying the increase of albumin permeability are probably due to endothelial cell damage as an initial event, which was demonstrated by the decrease of Platelet endothelial cell adhesion molecule (PECAM-1 or CD31), while the podocytes' expressions of synaptopodin and podocin were normal.
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4 |
31191670
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Furthermore, these cells express the typical MSC markers CD73, CD90, and CD105.
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5 |
31191670
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Immunofluorescence-based stainings of sectioned 3D-NPCs revealed cells expressing the renal progenitor cell markers (SIX2 and PAX8), podocyte markers (Nephrin and Podocin), the endothelial marker (CD31), and mesenchymal markers (Vimentin and PDGFR-β).
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6 |
30841422
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The circulating levels of GLP-1/SDF-1α and protein levels of angiogenesis (VEGF/SDF-1α/CXCR4) and GLP-1R in kidney were progressively increased from groups 1 to 5, whereas circulating DPP4 activity exhibited an opposite pattern of SDF-1α among the groups (all p < 0.0001).
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7 |
30841422
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The protein expressions of oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptosis (Bax/caspase-3/PARP), fibrosis (Smad3/TGF-ß) and inflammation (TNF-α/NF-κB/MMP-2) and kidney injury score displayed an opposite pattern, whereas the protein expressions of TMP2, endothelial-cell markers (CD31/eNOS) and podocyte integrity biomarkers (podocin/ZO-1/synaptopodin) exhibited an identical pattern of RBF among the groups (all p < 0.001).
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8 |
30814628
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Protease-activated receptor 2 protects against VEGF inhibitor-induced glomerular endothelial and podocyte injury.
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9 |
30814628
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We have recently shown that activation of protease-activated receptor 2 (PAR2) by factor Xa exacerbated diabetic kidney disease.
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10 |
30814628
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However, the role of PAR2 in glomerular injury induced by VEGF blockade is not known.
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11 |
30814628
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Herein, we investigated the effect of the lack of PAR2 on VEGF inhibitor-induced glomerular injury.
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12 |
30814628
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Different from what we expected, administration of an anti-VEGF antibody in mice lacking PAR2 and eNOS exacerbated albuminuria and reduced the expression levels of CD31, pro-angiogenic VEGF, and angiogenesis-related chemokines in their kidneys.
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13 |
30814628
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Our results suggest that PAR2 is protective against VEGF inhibitor-induced glomerular endothelial and podocyte injury.
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14 |
30072040
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Herein we describe a detailed protocol for generation of an advanced 3-dimensional kidney cellular model using induced pluripotent stem cells, where differentiation and maturation of kidney progenitors and podocytes can be monitored in live cells due to CRISPR/Cas9-mediated fluorescent tagging of kidney lineage markers (SIX2 and NPHS1).
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15 |
30072040
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Using paraffin-embedded sectioning and whole-mount immunostaining, we demonstrated that organoids grown in suspension culture express key markers of kidney biology (WT1, ECAD, LTL, nephrin) and vasculature (CD31) within renal cortical structures with microvilli, tight junctions and podocyte foot processes visualized by electron microscopy.
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16 |
29660398
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We performed an immunohistochemical study using a panel of endothelial, myoid, mesenchymal and stem/progenitor markers, namely CD31, CD34, CD105 (endoglin), CD117/c-kit, nestin, desmin, α-smooth muscle actin (α-SMA) and the heavy chain of smooth muscle myosin (SMM).
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17 |
29660398
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We performed an immunohistochemical study using a panel of endothelial, myoid, mesenchymal and stem/progenitor markers, namely CD31, CD34, CD105 (endoglin), CD117/c-kit, nestin, desmin, α-smooth muscle actin (α-SMA) and the heavy chain of smooth muscle myosin (SMM).
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18 |
29660398
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The capsular SC/TCs had a strong CD34 and partial nestin and CD105 immunopositivity.
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19 |
29660398
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The capsular SC/TCs had a strong CD34 and partial nestin and CD105 immunopositivity.
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20 |
29660398
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Subcapsular and interstitial SC/TCs expressed c-kit, nestin, CD105, but also α-SMA and SMM, therefore having a myoid phenotype.
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21 |
29660398
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Subcapsular and interstitial SC/TCs expressed c-kit, nestin, CD105, but also α-SMA and SMM, therefore having a myoid phenotype.
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22 |
29660398
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The endothelial SC/TCs phenotype was CD31+/CD34+/CD105+/nestin±/SMM±/α-SMA±.
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23 |
29660398
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The endothelial SC/TCs phenotype was CD31+/CD34+/CD105+/nestin±/SMM±/α-SMA±.
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24 |
29660398
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In epithelial cells, we found a positive expression for CD31, CD117/c-kit, desmin, CD34, SMM, and CD105.
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25 |
29660398
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In epithelial cells, we found a positive expression for CD31, CD117/c-kit, desmin, CD34, SMM, and CD105.
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26 |
28674043
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In FSGS-SCID mice, human Muse cells preferentially integrated into the damaged glomeruli and spontaneously differentiated into cells expressing markers of podocytes (podocin; 31%), mesangial cells (megsin; 13%), and endothelial cells (CD31; 41%) without fusing to the host cells; attenuated glomerular sclerosis and interstitial fibrosis; and induced the recovery of creatinine clearance at 7 weeks.
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27 |
27695940
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Both MET and EMT processes involve changes in content and organization of cytoskeletal and actin filaments, accompanied by the increased glomerular vascularization.
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28 |
27695940
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Here, we analyze and compare normal human developing, postnatal and nephrotic podocytes and glomeruli, using immunohistochemical and double immunofluorescent methods for detection of markers of cytoskeletal filaments (nestin, cytokeratin 10-CK10, vimentin and α-SMA), vasculogenesis (CD31 and VEGF) and podocyte function (receptor for advanced glycation end products, RAGE).
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29 |
27695940
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In differentiating podocytes and cells of Bowman's capsule (parietal podocytes) nestin decreases, vimentin increases, while CK10 gradually disappears.
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30 |
25859060
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We previously provided evidence that an apparent decrease in nephrin, caused by tensin2-deficiencient states, leads to podocytopathy, albuminuria and eventually, chronic renal failure.
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31 |
25859060
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We previously provided evidence that an apparent decrease in nephrin, caused by tensin2-deficiencient states, leads to podocytopathy, albuminuria and eventually, chronic renal failure.
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32 |
25859060
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Herein, we examined the changes of glomerular ECs, with focus on the expression of PECAM-1 and VE-cadherin (EC-specific markers), or of α-SMA (myofibroblast marker) in this mouse model by histological methods.
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33 |
25859060
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Herein, we examined the changes of glomerular ECs, with focus on the expression of PECAM-1 and VE-cadherin (EC-specific markers), or of α-SMA (myofibroblast marker) in this mouse model by histological methods.
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34 |
25859060
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Compared with the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the reduced expression of PECAM-1, or of VE-cadherin, in glomerular area.
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35 |
25859060
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Compared with the non-nephrotic (+/nep) mice, the nephrotic (nep/nep) mice exhibited the reduced expression of PECAM-1, or of VE-cadherin, in glomerular area.
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36 |
20818613
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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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37 |
20818613
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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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38 |
20818613
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Mature podocytes expressing WT1, Nestin, and Synaptopodin were observed from the mid-third trimester through adulthood.
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39 |
20818613
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Mature podocytes expressing WT1, Nestin, and Synaptopodin were observed from the mid-third trimester through adulthood.
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40 |
20818613
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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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41 |
20818613
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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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42 |
19759270
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CD31 and WT-1 localization was examined using immunohistochemistry and VEGF was localized using in situ hybridization.
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43 |
19579288
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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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44 |
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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45 |
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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46 |
19579288
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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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47 |
17464107
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In order to determine the characteristics of human glomerular development, we investigated the process of glomerular development by staining fetal and infant kidneys for CD31, CD34 and FB21, markers for endothelial cells, alpha-smooth muscle actin (alpha-SMA), a marker for mesangial cells, and nephrin, a marker for podocytes.
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48 |
17464107
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In order to determine the characteristics of human glomerular development, we investigated the process of glomerular development by staining fetal and infant kidneys for CD31, CD34 and FB21, markers for endothelial cells, alpha-smooth muscle actin (alpha-SMA), a marker for mesangial cells, and nephrin, a marker for podocytes.
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49 |
17464107
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In order to determine the characteristics of human glomerular development, we investigated the process of glomerular development by staining fetal and infant kidneys for CD31, CD34 and FB21, markers for endothelial cells, alpha-smooth muscle actin (alpha-SMA), a marker for mesangial cells, and nephrin, a marker for podocytes.
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50 |
17464107
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In each group, glomerular development was classified according to the developmental stage and the staining patterns for CD31, CD34, FB21, alpha-SMA and nephrin.
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51 |
17464107
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In each group, glomerular development was classified according to the developmental stage and the staining patterns for CD31, CD34, FB21, alpha-SMA and nephrin.
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52 |
17464107
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In each group, glomerular development was classified according to the developmental stage and the staining patterns for CD31, CD34, FB21, alpha-SMA and nephrin.
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53 |
17464107
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The staining patterns for CD31, CD34 and FB21 were similar in endothelial cells after 25 weeks of gestation.
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54 |
17464107
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The staining patterns for CD31, CD34 and FB21 were similar in endothelial cells after 25 weeks of gestation.
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55 |
17464107
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The staining patterns for CD31, CD34 and FB21 were similar in endothelial cells after 25 weeks of gestation.
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56 |
16773315
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TR-LE cells expressed lymphatic endothelial markers VEGFR-3 (vascular endothelial growth factor receptor), LYVE-1 (a lymphatic endothelial receptor), Prox-1 (a homeobox gene product), and podoplanin (a glomerular podocyte membrane mucoprotein), together with endothelial markers CD31, Tie-2, and VEGFR-2, whereas TR-BE cells expressed CD31, Tie-2, and VEGFR-2, but no lymphatic endothelial markers.
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57 |
16571784
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Differential expression of the intermediate filament protein nestin during renal development and its localization in adult podocytes.
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58 |
16571784
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Nestin, an intermediate filament protein, is widely used as stem cell marker.
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59 |
16571784
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The nestin-positive structures also were labeled by endothelial cell markers FLK1 and CD31 in immature glomeruli.
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60 |
16571784
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In contrast, in mature glomerular, nestin immunoreactivity was observed only outside laminin-positive glomerular basement membrane, and co-localized with nephrin, consistent with podocyte nestin expression.
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61 |
15220208
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Tumstatin peptide is an angiogenesis inhibitor derived from type IV collagen and inhibits in vivo neovascularization induced by vascular endothelial growth factor (VEGF), one of the mediators of glomerular hypertrophy in diabetic nephropathy.
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62 |
15220208
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Glomerular matrix expansion, the increase of total glomerular cell number and glomerular endothelial cells (CD31 positive), and monocyte/macrophage accumulation was inhibited by tumstatin peptide.
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63 |
15220208
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Increase in renal expression of VEGF, flk-1, and angiopoietin-2, an antagonist of angiopoietin-1, was inhibited by tumstatin treatment in diabetic mice.
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64 |
15220208
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Alteration of glomerular nephrin expression, a podocyte protein crucial for maintaining glomerular filtration barrier, was recovered by tumstatin in diabetic mice.
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65 |
10027397
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In normal skin and kidney, podoplanin colocalized with vascular endothelial growth factor receptor-3, the only other lymphatic marker presently available.
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66 |
10027397
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Complementary immunostaining of blood vessels was obtained with established endothelial markers (CD31, CD34, factor VIII-related antigen, and Ulex europaeus I lectin) as well as podocalyxin, another podocytic protein that is also localized in endothelia of blood vessels.
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67 |
9263995
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Concomitantly, the expression of IL-1 receptor type I (IL-1 RI), IL-1 receptor type II (IL-1 RII) and of IL-1 receptor antagonist (IL-1 RA) was analyzed.
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68 |
9263995
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Antibodies against antigens expressed on podocytes (PP-44), endothelial cells (CD31) and monocytes/macrophages (CD11b, CD14, CD68) were applied to attribute the expression of IL-1/IL-1 related peptides to intrinsic glomerular and/or blood-derived infiltrating cells.
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69 |
9263995
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In MGN and MCD/FSGS, the expression of both IL-1 forms is particularly noted in early stages of the disease and is not only accompanied by a marked reactivity for IL-1 RI, but also for IL-1 RA.
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70 |
9263995
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In segmental sclerosing lesions in FSGS and in IgA-GN with marked glomerular proliferation and/or sclerosis, a reduced expression of the PP-44 antigen and a diminished ability of podocytes to produce IL-1/IL-1 related peptides are noted.
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