thromboplastin and Glomerulonephritis--Membranoproliferative

thromboplastin has been researched along with Glomerulonephritis--Membranoproliferative* in 1 studies

Other Studies

1 other study(ies) available for thromboplastin and Glomerulonephritis--Membranoproliferative

Article	Year
Lipopolysaccharide-triggered acute aggravation of mesangioproliferative glomerulonephritis through activation of coagulation in a high IgA strain of ddY mice. Nephron. Experimental nephrology, 2009, Volume: 112, Issue:4 The high IgA (HIGA) strain of ddY mice represents an inbred model of IgA nephropathy that shows mesangioproliferative glomerulonephritis with mesangial IgA deposition. In this study, aggravation of glomerulonephritis in HIGA mice through lipopolysaccharide (LPS)-triggered activation of coagulation was investigated.. Twelve-week-old HIGA and BALB/c mice were intraperitoneally injected with LPS twice at an interval of 3 days, and kidney specimens were collected 7 days after the second LPS injection. In an intervention experiment, the factor Xa inhibitor danaparoid was injected intraperitoneally every day for 7 days after the first LPS injection.. LPS injection induced macrophage infiltration and cellular proliferation in the mesangium together with fibrin deposition and monocyte chemoattractant protein 1 mRNA expression, as well as antigen deposition of tissue factor, factor V, factor X, and protease-activated receptor 2. These phenomena were obvious in HIGA mice when compared to BALB/c mice. Interestingly, toll-like receptor 4 was intensely expressed in HIGA mice before LPS injection and subsequently decreased. Danaparoid treatment significantly ameliorated proteinuria, cellular proliferation, and fibrin deposition.. The present data suggest that tissue factor and factor V induction by LPS may in part accelerate mesangioproliferative glomerulonephritis through activation of factor X and downstream proinflammatory and procoagulant mechanisms. Topics: Animals; Anticoagulants; Blood Coagulation; Blotting, Western; Chemokine CCL2; Chondroitin Sulfates; Dermatan Sulfate; Factor V; Factor X; Female; Fibrin; Gene Expression; Glomerular Mesangium; Glomerulonephritis, Membranoproliferative; Heparitin Sulfate; Immunoglobulin A; Immunohistochemistry; Injections, Intraperitoneal; Lipopolysaccharides; Mice; Mice, Inbred BALB C; Microscopy, Fluorescence; Proliferating Cell Nuclear Antigen; Receptor, PAR-2; Reverse Transcriptase Polymerase Chain Reaction; Thromboplastin; Toll-Like Receptor 4	2009

Article

Year

Lipopolysaccharide-triggered acute aggravation of mesangioproliferative glomerulonephritis through activation of coagulation in a high IgA strain of ddY mice.

Nephron. Experimental nephrology, 2009, Volume: 112, Issue:4

The high IgA (HIGA) strain of ddY mice represents an inbred model of IgA nephropathy that shows mesangioproliferative glomerulonephritis with mesangial IgA deposition. In this study, aggravation of glomerulonephritis in HIGA mice through lipopolysaccharide (LPS)-triggered activation of coagulation was investigated.. Twelve-week-old HIGA and BALB/c mice were intraperitoneally injected with LPS twice at an interval of 3 days, and kidney specimens were collected 7 days after the second LPS injection. In an intervention experiment, the factor Xa inhibitor danaparoid was injected intraperitoneally every day for 7 days after the first LPS injection.. LPS injection induced macrophage infiltration and cellular proliferation in the mesangium together with fibrin deposition and monocyte chemoattractant protein 1 mRNA expression, as well as antigen deposition of tissue factor, factor V, factor X, and protease-activated receptor 2. These phenomena were obvious in HIGA mice when compared to BALB/c mice. Interestingly, toll-like receptor 4 was intensely expressed in HIGA mice before LPS injection and subsequently decreased. Danaparoid treatment significantly ameliorated proteinuria, cellular proliferation, and fibrin deposition.. The present data suggest that tissue factor and factor V induction by LPS may in part accelerate mesangioproliferative glomerulonephritis through activation of factor X and downstream proinflammatory and procoagulant mechanisms.

Topics: Animals; Anticoagulants; Blood Coagulation; Blotting, Western; Chemokine CCL2; Chondroitin Sulfates; Dermatan Sulfate; Factor V; Factor X; Female; Fibrin; Gene Expression; Glomerular Mesangium; Glomerulonephritis, Membranoproliferative; Heparitin Sulfate; Immunoglobulin A; Immunohistochemistry; Injections, Intraperitoneal; Lipopolysaccharides; Mice; Mice, Inbred BALB C; Microscopy, Fluorescence; Proliferating Cell Nuclear Antigen; Receptor, PAR-2; Reverse Transcriptase Polymerase Chain Reaction; Thromboplastin; Toll-Like Receptor 4

2009