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PLATELET-COMPLEMENT INTERACTIONS IN MESANGIAL PROLIFERATIVE NEPHRITIS IN THE RAT
Author(s): JOHNSON RJ, PRITZL P, IIDA H, ALPERS CE
Source: AMERICAN JOURNAL OF PATHOLOGY    Volume: 138    Issue: 2    Pages: 313-321    Published: FEB 1991  
Times Cited: 83     References: 36     
Abstract: Complement has been reported to mediate mesangiolysis and glomerular hypercellularity in the rat in a model of glomerulonephritis (GN) induced with anti-Thy 1 antibody. To investigate the mechanism for the complement-mediated hypercellularity, the authors first determined if the effect of complement depletion was to inhibit cell proliferation or whether the effect was primarily to inhibit leukocyte infiltration. Rats depleted of complement with cobra venom factor (CVF) had 1) significantly less mesangiolysis than controls at day 5 (0.6 +/- 0.1 versus 3.4 +/- 0.4, scale 0 - 4+, P < 0.001); 2) less cell proliferation, as assessed by immunostaining for the proliferating cell nuclear antigen (PCNA)/cyclin, a cellcycle-dependent antigen (0.5 +/- 0.1 versus 2.4 +/- 0.7 cells/glomerular cross-section, P < 0.01); and 3) less leukocyte infiltration as assessed by immunohistochemical labeling (0.6 +/- 0.1 versus 1.9 +/- 0.3 cells/glomerular cross-section, P < 0.01). Because it was reported recently that platelets also mediate glomerular cell proliferation in this model, this study examined whether the mechanism for complement-mediated cell proliferation involved an effect on glomerular platelet localization. The glomerular uptake of In-111-labeled platelets was quantiated in normal and CVF-treated rats at 1, 4, 12, and 24 hours after induction of GN. Rats with anti-Thy 1 GN had substantial glomerular accumulation of platelets at all times studied, peaking at 4 hours (608 +/- 171 platelets per glomerulus). Complement depletion profoundly reduced glomerular platelet localization in anti-Thy 1 GN (mean < 35 platelets per glomerulus at all times studied, P < 0.05). Thus these studies demonstrate an important role for complement in mediating platelet localization in anti-Thy 1 GN, an effect that may account for the complement-dependent, neutrophil-independent glomerular hypercellularity in this model.
Document Type: Article
Language: English
Reprint Address: JOHNSON, RJ (reprint author), UNIV WASHINGTON, MED CTR, DEPT MED, DIV NEPHROL, MAIL STOP RM-11, SEATTLE, WA 98195 USA
Addresses:
1. UNIV WASHINGTON, MED CTR, DEPT PATHOL, SEATTLE, WA 98195 USA
Publisher: AMER SOC INVESTIGATIVE PATHOLOGY, INC, 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993
Subject Category: Pathology
IDS Number: EX434
ISSN: 0002-9440
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