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1 he circulation and deposit in the glomerular mesangium.
2 sCD89 was also detected in patient and mouse mesangium.
3 s favoring IgA1 deposition in the glomerular mesangium.
4  to the interposition of the interglomerular mesangium.
5 ontaining immune complexes in the glomerular mesangium.
6 on preferentially deposits in the glomerular mesangium.
7 l O-glycosylation deposits in the glomerular mesangium.
8  accumulation of extracellular matrix in the mesangium.
9 by the deposition of immune complexes in the mesangium.
10 ulation of extracellular matrix (ECM) in the mesangium.
11 mplexes with proliferation of the glomerular mesangium.
12 was increased, with marked expression in the mesangium.
13 ulation and/or after their deposition in the mesangium.
14 s involved in monocyte infiltration into the mesangium.
15 lar mesangium, and throughout the glomerular mesangium.
16 er, the primary damage is encountered in the mesangium.
17 nstitute a population of cells in glomerular mesangium.
18 lary route is enclosed within the glomerular mesangium.
19 deficient IgA1 [Tn(+)IgA1] in the glomerular mesangium.
20 mesangial matrix fractional volume per total mesangium (0.61 +/- 0.07 vs. 0.64 +/- 0.09).
21 consistently observed in vessel walls (54%), mesangium (77%), GBM (4%), and tubular basement membrane
22   CML was the major AGE detected in diabetic mesangium (96%), glomerular basement membranes (GBM) (42
23 athways involved in monocyte adhesion to the mesangium, a phenomenon presumably regulated by signal-t
24 ls for reconstitution of the intraglomerular mesangium after injury.
25      However, inflammation of the glomerular mesangium also participates in at least the early phase
26 ges in protein composition of the glomerular mesangium and basement membrane and the evidence that, i
27 tion of extracellular matrix proteins in the mesangium and basement membrane of the glomerulus and in
28 ), IgA immune complexes are deposited in the mesangium and drive inflammation and extracellular matri
29 e immune complexes deposit in the glomerular mesangium and induce the mesangioproliferative glomerulo
30 y decreased deposition of collagen IV in the mesangium and less beta-galactosidase staining, an indic
31                       IgG was present in the mesangium and peripheral capillary walls along with exce
32 merular cell types, including the glomerular mesangium and podocytes.
33 on of extracellular matrix in the glomerular mesangium and the interstitium.
34 or both was predominantly located within the mesangium and the renal interstitium.
35  laminin chains including beta1 chain in the mesangium and tubular basement membranes at 1, 2, 3, and
36 re probably representing the extraglomerular mesangium, and throughout the glomerular mesangium.
37 ffects of HG on fibronectin synthesis in the mesangium are mediated by the HBP possibly via hexosamin
38 ions between the podocytes, endothelium, and mesangium associated with the glomerular capillary bed t
39 s of the basement membrane, expansion of the mesangium because of increased matrix and accumulation o
40 ed 5-fold by day 7 and was identified in the mesangium by in situ hybridization.
41 loss and the mice develop capillary loop and mesangium degeneration with little evidence of glomerulo
42 ding to lipoprotein dysregulation, excessive mesangium expansion as well as inflammation in the glome
43 the controls, and further development of the mesangium failed.
44  anti-alpha8 integrin immunoliposomes to the mesangium following tail vein injection in mice.
45  glomerular endothelium, subendothelium, and mesangium in all kidneys removed due to chronic rejectio
46 esults suggest that high levels of HA in the mesangium in disease is a mechanism controlling the accu
47     In contrast, Smad6 is upregulated in the mesangium in human glomerular diseases and may be involv
48 he fraction of glomerular volume occupied by mesangium in kidney-biopsy specimens.
49    Perlecan, a HSPG normally confined to the mesangium in mature glomeruli, did not appear in the mut
50 flt-1 and KDR receptors are expressed in the mesangium in mesangioproliferative disease.
51 reserve cells resided in the extraglomerular mesangium in the JGA and were not renin-secreting cells,
52 In diabetic glomeruli, ILK expression in the mesangium is dramatically increased.
53                     The effect of NTS on the mesangium is due, in large part, to the glomerular injur
54  of these immune complexes in the glomerular mesangium, leading to kidney inflammation and scarring.
55   Injected immune complexes localized to the mesangium of apoJ/clusterin-deficient but not wild-type
56                                          The mesangium of immature glomeruli also expressed LacZ.
57  the uptake and processing by the glomerular mesangium of intravenously administered protein macromol
58 ement membranes with scant expression in the mesangium of older mice.
59 n increase in macrophage infiltration in the mesangium of ovariectomized ROP Os/+.
60 mune complexes are trapped in the glomerular mesangium of the kidney where they trigger localized inf
61 tics for targeting diseases that involve the mesangium of the kidney.
62 ticles of ~75 +/- 25-nm diameters target the mesangium of the kidney.
63 ffects of particle diameter on targeting the mesangium of the kidney.
64 normal ability to clear [125I]AHIgG from the mesangium over 72 hr.
65 EBF1 knockout mice, we deleted EBF1 from the mesangium/pericytes (Foxd1-cre) or podocytes (Podocin-cr
66 une complexes that deposit in the glomerular mesangium, producing progressive kidney injury.
67                Polymeric IgA deposits in the mesangium seem to have varied pathogenic potential, but
68  In the human kidney, it is localized in the mesangium, the proximal tubule, the thick ascending limb
69 ement membrane and the evidence that, in the mesangium, these are initiated by changes in glucose met
70 st to other mutants in which the loss of the mesangium was due to migration defects, and suggests tha
71            Fibrinogen staining of glomerular mesangium was seen in kidneys with chronic rejection.
72 rogressively enlarged glomeruli and expanded mesangium with diffuse and nodular expansion of mesangia