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Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis

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Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis. / Kluger, Malte A; Zahner, Gunther; Paust, Hans-Joachim; Schaper, Melanie; Magnus, Tim; Panzer, Ulf; Stahl, Rolf A K.

In: KIDNEY INT, Vol. 83, No. 5, 01.05.2013, p. 865-77.

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

Harvard

Kluger, MA, Zahner, G, Paust, H-J, Schaper, M, Magnus, T, Panzer, U & Stahl, RAK 2013, 'Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis', KIDNEY INT, vol. 83, no. 5, pp. 865-77. https://doi.org/10.1038/ki.2012.483

APA

Kluger, M. A., Zahner, G., Paust, H-J., Schaper, M., Magnus, T., Panzer, U., & Stahl, R. A. K. (2013). Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis. KIDNEY INT, 83(5), 865-77. https://doi.org/10.1038/ki.2012.483

Vancouver

Kluger MA, Zahner G, Paust H-J, Schaper M, Magnus T, Panzer U et al. Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis. KIDNEY INT. 2013 May 1;83(5):865-77. https://doi.org/10.1038/ki.2012.483

Bibtex

@article{0244648cc0f24979afde8b52ffc9f9aa,
title = "Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis",
abstract = "Matrix metalloproteinase 9 (MMP9) is a conditionally expressed enzyme and is upregulated in glomerulonephritis. Its function in these diseases, however, remains to be fully elucidated. The induction of nephrotoxic serum nephritis (NTN) in wild-type mice resulted in an upregulation of MMP9, followed by leukocyte infiltration, albuminuria, and subsequent renal failure. MMP9 deficiency ameliorated the course of NTN as indicated by reduced histological injury and reduced infiltration of proinflammatory macrophages. The chemotaxis of MMP9-deficient macrophages in vitro was impaired. Intrarenal macrophages isolated from the kidneys of nephritic MMP9 knockout mice still displayed the typical features of a proinflammatory phenotype and were indistinguishable from wild type-derived cells. Bone marrow transplantation restored renal tissue injury and macrophage recruitment when wild type-derived donor cells were transplanted onto MMP9-deficient mice prior to the induction of NTN. Thus, leukocyte-derived MMP9 mediates the recruitment of proinflammatory macrophages into kidneys during experimental crescentic glomerulonephritis.",
keywords = "Animals, Bone Marrow Transplantation, Cells, Cultured, Chemokines, Chemotaxis, Disease Models, Animal, Disease Progression, Glomerulonephritis, Inflammation Mediators, Leukocytes, Macrophages, Peritoneal, Male, Matrix Metalloproteinase 9, Mice, Mice, Inbred C57BL, Mice, Knockout, Nephrons, Phenotype, Time Factors",
author = "Kluger, {Malte A} and Gunther Zahner and Hans-Joachim Paust and Melanie Schaper and Tim Magnus and Ulf Panzer and Stahl, {Rolf A K}",
year = "2013",
month = may,
day = "1",
doi = "10.1038/ki.2012.483",
language = "English",
volume = "83",
pages = "865--77",
journal = "KIDNEY INT",
issn = "0085-2538",
publisher = "NATURE PUBLISHING GROUP",
number = "5",

}

RIS

TY - JOUR

T1 - Leukocyte-derived MMP9 is crucial for the recruitment of proinflammatory macrophages in experimental glomerulonephritis

AU - Kluger, Malte A

AU - Zahner, Gunther

AU - Paust, Hans-Joachim

AU - Schaper, Melanie

AU - Magnus, Tim

AU - Panzer, Ulf

AU - Stahl, Rolf A K

PY - 2013/5/1

Y1 - 2013/5/1

N2 - Matrix metalloproteinase 9 (MMP9) is a conditionally expressed enzyme and is upregulated in glomerulonephritis. Its function in these diseases, however, remains to be fully elucidated. The induction of nephrotoxic serum nephritis (NTN) in wild-type mice resulted in an upregulation of MMP9, followed by leukocyte infiltration, albuminuria, and subsequent renal failure. MMP9 deficiency ameliorated the course of NTN as indicated by reduced histological injury and reduced infiltration of proinflammatory macrophages. The chemotaxis of MMP9-deficient macrophages in vitro was impaired. Intrarenal macrophages isolated from the kidneys of nephritic MMP9 knockout mice still displayed the typical features of a proinflammatory phenotype and were indistinguishable from wild type-derived cells. Bone marrow transplantation restored renal tissue injury and macrophage recruitment when wild type-derived donor cells were transplanted onto MMP9-deficient mice prior to the induction of NTN. Thus, leukocyte-derived MMP9 mediates the recruitment of proinflammatory macrophages into kidneys during experimental crescentic glomerulonephritis.

AB - Matrix metalloproteinase 9 (MMP9) is a conditionally expressed enzyme and is upregulated in glomerulonephritis. Its function in these diseases, however, remains to be fully elucidated. The induction of nephrotoxic serum nephritis (NTN) in wild-type mice resulted in an upregulation of MMP9, followed by leukocyte infiltration, albuminuria, and subsequent renal failure. MMP9 deficiency ameliorated the course of NTN as indicated by reduced histological injury and reduced infiltration of proinflammatory macrophages. The chemotaxis of MMP9-deficient macrophages in vitro was impaired. Intrarenal macrophages isolated from the kidneys of nephritic MMP9 knockout mice still displayed the typical features of a proinflammatory phenotype and were indistinguishable from wild type-derived cells. Bone marrow transplantation restored renal tissue injury and macrophage recruitment when wild type-derived donor cells were transplanted onto MMP9-deficient mice prior to the induction of NTN. Thus, leukocyte-derived MMP9 mediates the recruitment of proinflammatory macrophages into kidneys during experimental crescentic glomerulonephritis.

KW - Animals

KW - Bone Marrow Transplantation

KW - Cells, Cultured

KW - Chemokines

KW - Chemotaxis

KW - Disease Models, Animal

KW - Disease Progression

KW - Glomerulonephritis

KW - Inflammation Mediators

KW - Leukocytes

KW - Macrophages, Peritoneal

KW - Male

KW - Matrix Metalloproteinase 9

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Nephrons

KW - Phenotype

KW - Time Factors

U2 - 10.1038/ki.2012.483

DO - 10.1038/ki.2012.483

M3 - SCORING: Journal article

C2 - 23344471

VL - 83

SP - 865

EP - 877

JO - KIDNEY INT

JF - KIDNEY INT

SN - 0085-2538

IS - 5

ER -