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mesangial cell
Histological examination showed cell swelling, break-down and massive lipid deposition in renal tubules; perivascular and interstitial cell infiltration and mesangial cell proliferation.
      
A metabolic (WST-1) assay was used to measure mesangial cell proliferation and Western blot analysis was used to measure MMPs expression of mesangial cells.
      
Results Normal human mesangial cell (NHMC) proliferation was higher in high glucose (HG) medium than in low glucose (LG) medium.
      
Conclusions This study suggests that glucose can accelerate mesangial cell proliferation while heparin can reduce proliferation, being more obvious at high glucose concentrations.
      
Finally, various antioxidants inhibit mesangial cell activation by HG and ameliorate features of diabetic nephropathy.
      
In parallel to clinical studies searching for a mesangial autoantigen these experiments might help to elucidate the mechanisms of initiation and perpetuation of mesangial cell-dependent autoimmune glomerulonephritis.
      
Increasing evidence supports a role for glomerular mesangial cell proliferation and overproduction of extracellular matrix by mesangial cells in the development of focal or diffuse glomerulosclerosis.
      
In these experimental models, mesangial cell activation can be demonstrated early in the course of disease as exemplified by the de novo expression by the mesangial cell of a smooth muscle "specific" actin isotype (i.e., α-smooth muscle actin).
      
Following mesangial cell activation, cellular proliferation ensues both in the acute anti-Thy 1.1 model and, to a lesser degree, in the chronic remnant kidney model.
      
While a multitude of mitogens for mesangial cells has been proposed on the basis of in vitro experiments, the factors involved in the regulation of mesangial cell proliferation in vivo remain largely undefined.
      
In vivo studies show that PDGF, bFGF, and TGF-β participate in the mesangial cell proliferation and/or the mesangial matrix expansion that follows mesangial cell injury with anti-Thy 1.1 antibody.
      
Preliminary evidence also suggests the participation of some of these factors in the mesangial cell proliferation and matrix accumulation that is present in chronic glomerular disease such as in the remnant kidney model.
      
Prominent reactions in glomerular disease are mesangial expansion and progressive glomerular sclerosis, which are preceded by or associated with mesangial cell hypertrophy and/or proliferation.
      
Further identification of such mediators in situ will improve our understanding of pathological glomerular processes, particularly with respect to the multifunctional properties of the mesangial cell.
      
Retinoids, derivatives of vitamin A, inhibit mesangial cell proliferation, glomerular inflammation, and extracellular matrix deposition in acute anti-Thy1.1 glomerulonephritis (Thy-GN) of the rat.
      
Although similar findings developed progressively with age, mesangial cell alterations, coalescence and cystic dilatation and fusion of capillary loops in the glomeruli of young hamsters were characteristic findings of diabetic glomerulopathy.
      
An analogy was suggested between the dilatation and coalescence of glomerular capillaries associated with mesangial cell changes and the dilatation of retinal capillaries associated with degeneration of the supporting mural cells in man.
      
Increase in the total mesangial cell volume per glomerulus by 46 and 43% (2p = 0.033 and 0.048); 4.
      
These results indicate the importance of glucose-induced alteration of mesangial cell function in the development of diabetic mesangial expansion.
      
Hybridization of mesangial cell mRNA with cDNA probes revealed transcripts for the Na+/glucose co-transporter as well as GLUT1 and to a lesser extent GLUT4.
      
 

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