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, Jahrgang 83, Nr. 5, 01.05.2013, S. 865-77.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -