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Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis

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Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis. / Hohenstein, Bernd; Kasperek, Laura; Kobelt, Dieter-Johannes; Daniel, Christoph; Gambaryan, Stepan; Renné, Thomas; Walter, Ulrich; Amann, Kerstin U; Hugo, Christian P M.

In: J AM SOC NEPHROL, Vol. 16, No. 4, 01.04.2005, p. 986-96.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hohenstein, B, Kasperek, L, Kobelt, D-J, Daniel, C, Gambaryan, S, Renné, T, Walter, U, Amann, KU & Hugo, CPM 2005, 'Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis', J AM SOC NEPHROL, vol. 16, no. 4, pp. 986-96. https://doi.org/10.1681/ASN.2004070591

APA

Hohenstein, B., Kasperek, L., Kobelt, D-J., Daniel, C., Gambaryan, S., Renné, T., Walter, U., Amann, K. U., & Hugo, C. P. M. (2005). Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis. J AM SOC NEPHROL, 16(4), 986-96. https://doi.org/10.1681/ASN.2004070591

Vancouver

Hohenstein B, Kasperek L, Kobelt D-J, Daniel C, Gambaryan S, Renné T et al. Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis. J AM SOC NEPHROL. 2005 Apr 1;16(4):986-96. https://doi.org/10.1681/ASN.2004070591

Bibtex

@article{7c2efee2326b4043ae39260b8084aff5,
title = "Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis",
abstract = "Vasodilator-stimulated phosphoprotein (VASP), an actin cytoskeletal protein, is expressed in various cell types including renal cells. In vitro studies provide evidence for a role of VASP regarding platelet activation, cell adhesion, migration, and capillary formation. The in vivo role of VASP was investigated in experimental inflammatory renal disease. Kidneys of healthy VASP deficient (-/-) and wild-type (wt) mice were compared regarding morphology and functional parameters. Passive nephrotoxic nephritis was induced in 28 VASP -/- and 28 wt mice; kidneys were harvested; and tissues were analyzed by morphometric, immunohistochemical, and electron microscopic techniques on days 3, 7, 14, and 28. The time course of disease in VASP -/- mice differed substantially and biphasically from that in wt controls. Early on, VASP -/- mice demonstrated increased platelet influx associated with augmented glomerular and tubulointerstitial inflammation and sclerosis. Whereas renal disease continuously worsened up to day 28 in wt controls, renal disease in VASP -/- mice hardly progressed after day 3 as assessed by various injury indices. This long-term improvement of renal histology in VASP -/- compared with wt mice was associated with remarkable capillary preservation/regeneration up to day 28 mediated via an increased proliferative and a reduced apoptotic activity of VASP-negative peritubular endothelial cells. Despite an enhanced injury response early on, VASP -/- mice are protected from long-term progression of nephrotoxic nephritis, which is associated with improved renal endothelial cell preservation and regeneration.",
keywords = "Animals, Antibodies, Capillaries, Cell Adhesion Molecules, Disease Progression, Endothelium, Vascular, Kidney, Mice, Mice, Knockout, Microfilament Proteins, Nephritis, Phosphoproteins, Platelet Activation, Up-Regulation",
author = "Bernd Hohenstein and Laura Kasperek and Dieter-Johannes Kobelt and Christoph Daniel and Stepan Gambaryan and Thomas Renn{\'e} and Ulrich Walter and Amann, {Kerstin U} and Hugo, {Christian P M}",
year = "2005",
month = apr,
day = "1",
doi = "10.1681/ASN.2004070591",
language = "English",
volume = "16",
pages = "986--96",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "4",

}

RIS

TY - JOUR

T1 - Vasodilator-stimulated phosphoprotein-deficient mice demonstrate increased platelet activation but improved renal endothelial preservation and regeneration in passive nephrotoxic nephritis

AU - Hohenstein, Bernd

AU - Kasperek, Laura

AU - Kobelt, Dieter-Johannes

AU - Daniel, Christoph

AU - Gambaryan, Stepan

AU - Renné, Thomas

AU - Walter, Ulrich

AU - Amann, Kerstin U

AU - Hugo, Christian P M

PY - 2005/4/1

Y1 - 2005/4/1

N2 - Vasodilator-stimulated phosphoprotein (VASP), an actin cytoskeletal protein, is expressed in various cell types including renal cells. In vitro studies provide evidence for a role of VASP regarding platelet activation, cell adhesion, migration, and capillary formation. The in vivo role of VASP was investigated in experimental inflammatory renal disease. Kidneys of healthy VASP deficient (-/-) and wild-type (wt) mice were compared regarding morphology and functional parameters. Passive nephrotoxic nephritis was induced in 28 VASP -/- and 28 wt mice; kidneys were harvested; and tissues were analyzed by morphometric, immunohistochemical, and electron microscopic techniques on days 3, 7, 14, and 28. The time course of disease in VASP -/- mice differed substantially and biphasically from that in wt controls. Early on, VASP -/- mice demonstrated increased platelet influx associated with augmented glomerular and tubulointerstitial inflammation and sclerosis. Whereas renal disease continuously worsened up to day 28 in wt controls, renal disease in VASP -/- mice hardly progressed after day 3 as assessed by various injury indices. This long-term improvement of renal histology in VASP -/- compared with wt mice was associated with remarkable capillary preservation/regeneration up to day 28 mediated via an increased proliferative and a reduced apoptotic activity of VASP-negative peritubular endothelial cells. Despite an enhanced injury response early on, VASP -/- mice are protected from long-term progression of nephrotoxic nephritis, which is associated with improved renal endothelial cell preservation and regeneration.

AB - Vasodilator-stimulated phosphoprotein (VASP), an actin cytoskeletal protein, is expressed in various cell types including renal cells. In vitro studies provide evidence for a role of VASP regarding platelet activation, cell adhesion, migration, and capillary formation. The in vivo role of VASP was investigated in experimental inflammatory renal disease. Kidneys of healthy VASP deficient (-/-) and wild-type (wt) mice were compared regarding morphology and functional parameters. Passive nephrotoxic nephritis was induced in 28 VASP -/- and 28 wt mice; kidneys were harvested; and tissues were analyzed by morphometric, immunohistochemical, and electron microscopic techniques on days 3, 7, 14, and 28. The time course of disease in VASP -/- mice differed substantially and biphasically from that in wt controls. Early on, VASP -/- mice demonstrated increased platelet influx associated with augmented glomerular and tubulointerstitial inflammation and sclerosis. Whereas renal disease continuously worsened up to day 28 in wt controls, renal disease in VASP -/- mice hardly progressed after day 3 as assessed by various injury indices. This long-term improvement of renal histology in VASP -/- compared with wt mice was associated with remarkable capillary preservation/regeneration up to day 28 mediated via an increased proliferative and a reduced apoptotic activity of VASP-negative peritubular endothelial cells. Despite an enhanced injury response early on, VASP -/- mice are protected from long-term progression of nephrotoxic nephritis, which is associated with improved renal endothelial cell preservation and regeneration.

KW - Animals

KW - Antibodies

KW - Capillaries

KW - Cell Adhesion Molecules

KW - Disease Progression

KW - Endothelium, Vascular

KW - Kidney

KW - Mice

KW - Mice, Knockout

KW - Microfilament Proteins

KW - Nephritis

KW - Phosphoproteins

KW - Platelet Activation

KW - Up-Regulation

U2 - 10.1681/ASN.2004070591

DO - 10.1681/ASN.2004070591

M3 - SCORING: Journal article

C2 - 15743999

VL - 16

SP - 986

EP - 996

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 4

ER -