CD44 is required for the pathogenesis of experimental crescentic glomerulonephritis and collapsing focal segmental glomerulosclerosis
A key feature of glomerular diseases such as crescentic glomerulonephritis and focal segmental glomerulosclerosis is the activation, migration and proliferation of parietal epithelial cells. CD44-positive activated parietal epithelial cells have been identified in proliferative cellular lesions in g...
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| Veröffentlicht in: | Kidney international Jg. 93; H. 3; S. 626 |
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01.03.2018
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| Abstract | A key feature of glomerular diseases such as crescentic glomerulonephritis and focal segmental glomerulosclerosis is the activation, migration and proliferation of parietal epithelial cells. CD44-positive activated parietal epithelial cells have been identified in proliferative cellular lesions in glomerular disease. However, it remains unknown whether CD44-positive parietal epithelial cells contribute to the pathogenesis of scarring glomerular diseases. Here, we evaluated this in experimental crescentic glomerulonephritis and the transgenic anti-Thy1.1 model for collapsing focal segmental glomerulosclerosis in CD44-deficient (cd44-/-) and wild type mice. For both models albuminuria was significantly lower in cd44-/- compared to wild type mice. The number of glomerular Ki67-positive proliferating cells was significantly reduced in cd44-/- compared to wild type mice, which was associated with a reduced number of glomerular lesions in crescentic glomerulonephritis. In collapsing focal segmental glomerulosclerosis, the extracapillary proliferative cellular lesions were smaller in cd44-/- mice, but the number of glomerular lesions was not different compared to wild type mice. For crescentic glomerulonephritis the influx of granulocytes and macrophages into the glomerulus was similar. In vitro, the growth of CD44-deficient murine parietal epithelial cells was reduced compared to wild type parietal epithelial cells, and human parietal epithelial cell migration could be inhibited using antibodies directed against CD44. Thus, CD44-positive proliferating glomerular cells, most likely parietal epithelial cells, are essential in the pathogenesis of scarring glomerular disease. |
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| AbstractList | A key feature of glomerular diseases such as crescentic glomerulonephritis and focal segmental glomerulosclerosis is the activation, migration and proliferation of parietal epithelial cells. CD44-positive activated parietal epithelial cells have been identified in proliferative cellular lesions in glomerular disease. However, it remains unknown whether CD44-positive parietal epithelial cells contribute to the pathogenesis of scarring glomerular diseases. Here, we evaluated this in experimental crescentic glomerulonephritis and the transgenic anti-Thy1.1 model for collapsing focal segmental glomerulosclerosis in CD44-deficient (cd44-/-) and wild type mice. For both models albuminuria was significantly lower in cd44-/- compared to wild type mice. The number of glomerular Ki67-positive proliferating cells was significantly reduced in cd44-/- compared to wild type mice, which was associated with a reduced number of glomerular lesions in crescentic glomerulonephritis. In collapsing focal segmental glomerulosclerosis, the extracapillary proliferative cellular lesions were smaller in cd44-/- mice, but the number of glomerular lesions was not different compared to wild type mice. For crescentic glomerulonephritis the influx of granulocytes and macrophages into the glomerulus was similar. In vitro, the growth of CD44-deficient murine parietal epithelial cells was reduced compared to wild type parietal epithelial cells, and human parietal epithelial cell migration could be inhibited using antibodies directed against CD44. Thus, CD44-positive proliferating glomerular cells, most likely parietal epithelial cells, are essential in the pathogenesis of scarring glomerular disease.A key feature of glomerular diseases such as crescentic glomerulonephritis and focal segmental glomerulosclerosis is the activation, migration and proliferation of parietal epithelial cells. CD44-positive activated parietal epithelial cells have been identified in proliferative cellular lesions in glomerular disease. However, it remains unknown whether CD44-positive parietal epithelial cells contribute to the pathogenesis of scarring glomerular diseases. Here, we evaluated this in experimental crescentic glomerulonephritis and the transgenic anti-Thy1.1 model for collapsing focal segmental glomerulosclerosis in CD44-deficient (cd44-/-) and wild type mice. For both models albuminuria was significantly lower in cd44-/- compared to wild type mice. The number of glomerular Ki67-positive proliferating cells was significantly reduced in cd44-/- compared to wild type mice, which was associated with a reduced number of glomerular lesions in crescentic glomerulonephritis. In collapsing focal segmental glomerulosclerosis, the extracapillary proliferative cellular lesions were smaller in cd44-/- mice, but the number of glomerular lesions was not different compared to wild type mice. For crescentic glomerulonephritis the influx of granulocytes and macrophages into the glomerulus was similar. In vitro, the growth of CD44-deficient murine parietal epithelial cells was reduced compared to wild type parietal epithelial cells, and human parietal epithelial cell migration could be inhibited using antibodies directed against CD44. Thus, CD44-positive proliferating glomerular cells, most likely parietal epithelial cells, are essential in the pathogenesis of scarring glomerular disease. A key feature of glomerular diseases such as crescentic glomerulonephritis and focal segmental glomerulosclerosis is the activation, migration and proliferation of parietal epithelial cells. CD44-positive activated parietal epithelial cells have been identified in proliferative cellular lesions in glomerular disease. However, it remains unknown whether CD44-positive parietal epithelial cells contribute to the pathogenesis of scarring glomerular diseases. Here, we evaluated this in experimental crescentic glomerulonephritis and the transgenic anti-Thy1.1 model for collapsing focal segmental glomerulosclerosis in CD44-deficient (cd44-/-) and wild type mice. For both models albuminuria was significantly lower in cd44-/- compared to wild type mice. The number of glomerular Ki67-positive proliferating cells was significantly reduced in cd44-/- compared to wild type mice, which was associated with a reduced number of glomerular lesions in crescentic glomerulonephritis. In collapsing focal segmental glomerulosclerosis, the extracapillary proliferative cellular lesions were smaller in cd44-/- mice, but the number of glomerular lesions was not different compared to wild type mice. For crescentic glomerulonephritis the influx of granulocytes and macrophages into the glomerulus was similar. In vitro, the growth of CD44-deficient murine parietal epithelial cells was reduced compared to wild type parietal epithelial cells, and human parietal epithelial cell migration could be inhibited using antibodies directed against CD44. Thus, CD44-positive proliferating glomerular cells, most likely parietal epithelial cells, are essential in the pathogenesis of scarring glomerular disease. |
| Author | Sharma, Shagun Ostendorf, Tammo van der Vlag, Johan Dijkman, Henry B Loeven, Markus A Wetzels, Jack F Sharma, Vikram Bakker, Marinka A Willemsen, Brigith K Deegens, Jeroen K Smeets, Bart Eymael, Jennifer Moeller, Marcus J van Kuppevelt, Toin H Florquin, Sandrine Mooren, Fieke |
| Author_xml | – sequence: 1 givenname: Jennifer surname: Eymael fullname: Eymael, Jennifer organization: Department of Pathology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 2 givenname: Shagun surname: Sharma fullname: Sharma, Shagun organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands; School of Biomedical and Healthcare Sciences, Plymouth University, Plymouth, UK – sequence: 3 givenname: Markus A surname: Loeven fullname: Loeven, Markus A organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 4 givenname: Jack F surname: Wetzels fullname: Wetzels, Jack F organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 5 givenname: Fieke surname: Mooren fullname: Mooren, Fieke organization: Department of Pathology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 6 givenname: Sandrine surname: Florquin fullname: Florquin, Sandrine organization: Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands – sequence: 7 givenname: Jeroen K surname: Deegens fullname: Deegens, Jeroen K organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 8 givenname: Brigith K surname: Willemsen fullname: Willemsen, Brigith K organization: Department of Pathology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 9 givenname: Vikram surname: Sharma fullname: Sharma, Vikram organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands; School of Biomedical and Healthcare Sciences, Plymouth University, Plymouth, UK – sequence: 10 givenname: Toin H surname: van Kuppevelt fullname: van Kuppevelt, Toin H organization: Department of Biochemistry, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 11 givenname: Marinka A surname: Bakker fullname: Bakker, Marinka A organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 12 givenname: Tammo surname: Ostendorf fullname: Ostendorf, Tammo organization: Division of Nephrology and Clinical Immunology, RWTH University of Aachen, Aachen, Germany – sequence: 13 givenname: Marcus J surname: Moeller fullname: Moeller, Marcus J organization: Division of Nephrology and Clinical Immunology, RWTH University of Aachen, Aachen, Germany – sequence: 14 givenname: Henry B surname: Dijkman fullname: Dijkman, Henry B organization: Department of Pathology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands – sequence: 15 givenname: Bart surname: Smeets fullname: Smeets, Bart email: Bart.Smeets@radboudumc.nl organization: Department of Pathology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands. Electronic address: Bart.Smeets@radboudumc.nl – sequence: 16 givenname: Johan surname: van der Vlag fullname: van der Vlag, Johan email: Johan.vanderVlag@radboudumc.nl organization: Department of Nephrology, RIMLS, RIHS, Radboud University Medical Center, Nijmegen, The Netherlands. Electronic address: Johan.vanderVlag@radboudumc.nl |
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| Copyright | Copyright © 2017 International Society of Nephrology. Published by Elsevier Inc. All rights reserved. |
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| Keywords | cell migration parietal epithelial cells collapsing FSGS crescentic glomerulonephritis CD44 |
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| SubjectTerms | Albuminuria - genetics Albuminuria - immunology Albuminuria - metabolism Animals Anti-Glomerular Basement Membrane Disease - genetics Anti-Glomerular Basement Membrane Disease - immunology Anti-Glomerular Basement Membrane Disease - metabolism Anti-Glomerular Basement Membrane Disease - pathology Autoantibodies - immunology Cell Movement Cell Proliferation Cells, Cultured Disease Models, Animal Epithelial Cells - immunology Epithelial Cells - metabolism Epithelial Cells - pathology Extracellular Matrix Proteins - metabolism Genetic Predisposition to Disease Glomerulosclerosis, Focal Segmental - genetics Glomerulosclerosis, Focal Segmental - immunology Glomerulosclerosis, Focal Segmental - metabolism Glomerulosclerosis, Focal Segmental - pathology Granulocytes - immunology Granulocytes - metabolism Hyaluronan Receptors - genetics Hyaluronan Receptors - immunology Hyaluronan Receptors - metabolism Kidney Glomerulus - immunology Kidney Glomerulus - metabolism Kidney Glomerulus - pathology Macrophages - immunology Macrophages - metabolism Mice, Inbred C57BL Mice, Knockout Phenotype Signal Transduction Thy-1 Antigens - genetics Thy-1 Antigens - immunology Thy-1 Antigens - metabolism |
| Title | CD44 is required for the pathogenesis of experimental crescentic glomerulonephritis and collapsing focal segmental glomerulosclerosis |
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