author_facet Caster, Dawn J.
Korte, Erik A.
Tan, Min
Barati, Michelle T.
Tandon, Shweta
Creed, T. Michael
Salant, David J.
Hata, Jessica L.
Epstein, Paul N.
Huang, Hui
Powell, David W.
McLeish, Kenneth R.
Caster, Dawn J.
Korte, Erik A.
Tan, Min
Barati, Michelle T.
Tandon, Shweta
Creed, T. Michael
Salant, David J.
Hata, Jessica L.
Epstein, Paul N.
Huang, Hui
Powell, David W.
McLeish, Kenneth R.
author Caster, Dawn J.
Korte, Erik A.
Tan, Min
Barati, Michelle T.
Tandon, Shweta
Creed, T. Michael
Salant, David J.
Hata, Jessica L.
Epstein, Paul N.
Huang, Hui
Powell, David W.
McLeish, Kenneth R.
spellingShingle Caster, Dawn J.
Korte, Erik A.
Tan, Min
Barati, Michelle T.
Tandon, Shweta
Creed, T. Michael
Salant, David J.
Hata, Jessica L.
Epstein, Paul N.
Huang, Hui
Powell, David W.
McLeish, Kenneth R.
American Journal of Physiology-Renal Physiology
Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
Physiology
author_sort caster, dawn j.
spelling Caster, Dawn J. Korte, Erik A. Tan, Min Barati, Michelle T. Tandon, Shweta Creed, T. Michael Salant, David J. Hata, Jessica L. Epstein, Paul N. Huang, Hui Powell, David W. McLeish, Kenneth R. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00039.2018 <jats:p>Acute glomerulonephritis is characterized by rapid glomerular neutrophil recruitment, proteinuria, and glomerular hypercellularity. The current study tested the hypothesis that the release of neutrophil granule contents plays a role in both the loss of filtration barrier leading to proteinuria and the increase in glomerular cells. Inhibition of neutrophil exocytosis with a peptide inhibitor prevented proteinuria and attenuated podocyte and endothelial cell injury but had no effect on glomerular hypercellularity in an experimental acute glomerulonephritis model in mice. Cultivation of podocytes with neutrophil granule contents disrupted cytoskeletal organization, an in vitro model for podocyte effacement and loss of filtration barrier. Activated, cultured podocytes released cytokines that stimulated neutrophil chemotaxis, primed respiratory burst activity, and stimulated neutrophil exocytosis. We conclude that crosstalk between podocytes and neutrophils contributes to disruption of the glomerular filtration barrier in acute glomerulonephritis. Neutrophil granule products induce podocyte injury but do not participate in the proliferative response of intrinsic glomerular cells.</jats:p> Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis American Journal of Physiology-Renal Physiology
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series American Journal of Physiology-Renal Physiology
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title Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_unstemmed Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_full Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_fullStr Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_full_unstemmed Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_short Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_sort neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
topic Physiology
url http://dx.doi.org/10.1152/ajprenal.00039.2018
publishDate 2018
physical F595-F606
description <jats:p>Acute glomerulonephritis is characterized by rapid glomerular neutrophil recruitment, proteinuria, and glomerular hypercellularity. The current study tested the hypothesis that the release of neutrophil granule contents plays a role in both the loss of filtration barrier leading to proteinuria and the increase in glomerular cells. Inhibition of neutrophil exocytosis with a peptide inhibitor prevented proteinuria and attenuated podocyte and endothelial cell injury but had no effect on glomerular hypercellularity in an experimental acute glomerulonephritis model in mice. Cultivation of podocytes with neutrophil granule contents disrupted cytoskeletal organization, an in vitro model for podocyte effacement and loss of filtration barrier. Activated, cultured podocytes released cytokines that stimulated neutrophil chemotaxis, primed respiratory burst activity, and stimulated neutrophil exocytosis. We conclude that crosstalk between podocytes and neutrophils contributes to disruption of the glomerular filtration barrier in acute glomerulonephritis. Neutrophil granule products induce podocyte injury but do not participate in the proliferative response of intrinsic glomerular cells.</jats:p>
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author Caster, Dawn J., Korte, Erik A., Tan, Min, Barati, Michelle T., Tandon, Shweta, Creed, T. Michael, Salant, David J., Hata, Jessica L., Epstein, Paul N., Huang, Hui, Powell, David W., McLeish, Kenneth R.
author_facet Caster, Dawn J., Korte, Erik A., Tan, Min, Barati, Michelle T., Tandon, Shweta, Creed, T. Michael, Salant, David J., Hata, Jessica L., Epstein, Paul N., Huang, Hui, Powell, David W., McLeish, Kenneth R., Caster, Dawn J., Korte, Erik A., Tan, Min, Barati, Michelle T., Tandon, Shweta, Creed, T. Michael, Salant, David J., Hata, Jessica L., Epstein, Paul N., Huang, Hui, Powell, David W., McLeish, Kenneth R.
author_sort caster, dawn j.
container_issue 3
container_start_page 0
container_title American Journal of Physiology-Renal Physiology
container_volume 315
description <jats:p>Acute glomerulonephritis is characterized by rapid glomerular neutrophil recruitment, proteinuria, and glomerular hypercellularity. The current study tested the hypothesis that the release of neutrophil granule contents plays a role in both the loss of filtration barrier leading to proteinuria and the increase in glomerular cells. Inhibition of neutrophil exocytosis with a peptide inhibitor prevented proteinuria and attenuated podocyte and endothelial cell injury but had no effect on glomerular hypercellularity in an experimental acute glomerulonephritis model in mice. Cultivation of podocytes with neutrophil granule contents disrupted cytoskeletal organization, an in vitro model for podocyte effacement and loss of filtration barrier. Activated, cultured podocytes released cytokines that stimulated neutrophil chemotaxis, primed respiratory burst activity, and stimulated neutrophil exocytosis. We conclude that crosstalk between podocytes and neutrophils contributes to disruption of the glomerular filtration barrier in acute glomerulonephritis. Neutrophil granule products induce podocyte injury but do not participate in the proliferative response of intrinsic glomerular cells.</jats:p>
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spelling Caster, Dawn J. Korte, Erik A. Tan, Min Barati, Michelle T. Tandon, Shweta Creed, T. Michael Salant, David J. Hata, Jessica L. Epstein, Paul N. Huang, Hui Powell, David W. McLeish, Kenneth R. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.00039.2018 <jats:p>Acute glomerulonephritis is characterized by rapid glomerular neutrophil recruitment, proteinuria, and glomerular hypercellularity. The current study tested the hypothesis that the release of neutrophil granule contents plays a role in both the loss of filtration barrier leading to proteinuria and the increase in glomerular cells. Inhibition of neutrophil exocytosis with a peptide inhibitor prevented proteinuria and attenuated podocyte and endothelial cell injury but had no effect on glomerular hypercellularity in an experimental acute glomerulonephritis model in mice. Cultivation of podocytes with neutrophil granule contents disrupted cytoskeletal organization, an in vitro model for podocyte effacement and loss of filtration barrier. Activated, cultured podocytes released cytokines that stimulated neutrophil chemotaxis, primed respiratory burst activity, and stimulated neutrophil exocytosis. We conclude that crosstalk between podocytes and neutrophils contributes to disruption of the glomerular filtration barrier in acute glomerulonephritis. Neutrophil granule products induce podocyte injury but do not participate in the proliferative response of intrinsic glomerular cells.</jats:p> Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis American Journal of Physiology-Renal Physiology
spellingShingle Caster, Dawn J., Korte, Erik A., Tan, Min, Barati, Michelle T., Tandon, Shweta, Creed, T. Michael, Salant, David J., Hata, Jessica L., Epstein, Paul N., Huang, Hui, Powell, David W., McLeish, Kenneth R., American Journal of Physiology-Renal Physiology, Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis, Physiology
title Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_full Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_fullStr Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_full_unstemmed Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_short Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_sort neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
title_unstemmed Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis
topic Physiology
url http://dx.doi.org/10.1152/ajprenal.00039.2018