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1 to the interposition of the interglomerular mesangium.
2 ontaining immune complexes in the glomerular mesangium.
3 ulation and/or after their deposition in the mesangium.
4 on preferentially deposits in the glomerular mesangium.
5 l O-glycosylation deposits in the glomerular mesangium.
6 nstitute a population of cells in glomerular mesangium.
7 accumulation of extracellular matrix in the mesangium.
8 by the deposition of immune complexes in the mesangium.
9 ulation of extracellular matrix (ECM) in the mesangium.
10 mplexes with proliferation of the glomerular mesangium.
11 was increased, with marked expression in the mesangium.
12 s involved in monocyte infiltration into the mesangium.
13 lar mesangium, and throughout the glomerular mesangium.
14 he circulation and deposit in the glomerular mesangium.
15 sCD89 was also detected in patient and mouse mesangium.
16 s favoring IgA1 deposition in the glomerular mesangium.
18 consistently observed in vessel walls (54%), mesangium (77%), GBM (4%), and tubular basement membrane
19 CML was the major AGE detected in diabetic mesangium (96%), glomerular basement membranes (GBM) (42
20 athways involved in monocyte adhesion to the mesangium, a phenomenon presumably regulated by signal-t
23 ges in protein composition of the glomerular mesangium and basement membrane and the evidence that, i
24 tion of extracellular matrix proteins in the mesangium and basement membrane of the glomerulus and in
25 e immune complexes deposit in the glomerular mesangium and induce the mesangioproliferative glomerulo
26 y decreased deposition of collagen IV in the mesangium and less beta-galactosidase staining, an indic
30 laminin chains including beta1 chain in the mesangium and tubular basement membranes at 1, 2, 3, and
32 ffects of HG on fibronectin synthesis in the mesangium are mediated by the HBP possibly via hexosamin
33 ions between the podocytes, endothelium, and mesangium associated with the glomerular capillary bed t
34 s of the basement membrane, expansion of the mesangium because of increased matrix and accumulation o
36 loss and the mice develop capillary loop and mesangium degeneration with little evidence of glomerulo
39 glomerular endothelium, subendothelium, and mesangium in all kidneys removed due to chronic rejectio
40 esults suggest that high levels of HA in the mesangium in disease is a mechanism controlling the accu
41 In contrast, Smad6 is upregulated in the mesangium in human glomerular diseases and may be involv
43 Perlecan, a HSPG normally confined to the mesangium in mature glomeruli, did not appear in the mut
45 reserve cells resided in the extraglomerular mesangium in the JGA and were not renin-secreting cells,
48 Injected immune complexes localized to the mesangium of apoJ/clusterin-deficient but not wild-type
50 the uptake and processing by the glomerular mesangium of intravenously administered protein macromol
53 mune complexes are trapped in the glomerular mesangium of the kidney where they trigger localized inf
59 In the human kidney, it is localized in the mesangium, the proximal tubule, the thick ascending limb
60 ement membrane and the evidence that, in the mesangium, these are initiated by changes in glucose met
61 st to other mutants in which the loss of the mesangium was due to migration defects, and suggests tha
63 rogressively enlarged glomeruli and expanded mesangium with diffuse and nodular expansion of mesangia
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