Glomerular Hypertension and Progressive Renal Disease: The Interplay of Mesangial Cell Stretch, Cytokine Formation and Extracellular Matrix Synthesis

2015 ◽  
pp. 229-233 ◽  
Author(s):  
Pedro Cortes ◽  
Bruce Riser ◽  
Robert G. Narins
Keyword(s):  
Extracellular Matrix ◽  
Renal Disease ◽  
Mesangial Cell ◽  
Matrix Synthesis ◽  
Cell Stretch ◽  
Glomerular Hypertension ◽  
Cytokine Formation ◽  
Progressive Renal Disease

Role of Mesangial Cell Damage in Progressive Renal Disease

1999 ◽  
Vol 22 (1-2) ◽  
pp. 5-12 ◽  
Author(s):  
F. Shimizu ◽  
H. Kawachi ◽  
M. Orikasa
Keyword(s):  
Renal Disease ◽  
Mesangial Cell ◽  
Cell Damage ◽  
Progressive Renal Disease

scholarly journals Production of an inhibitor of rat mesangial cell growth by the glomerulus and its alteration in puromycin nephrosis.

1993 ◽  
Vol 4 (2) ◽  
pp. 155-161
Author(s):  
G C Groggel ◽  
M L Hughes
Keyword(s):  
Cell Growth ◽  
Renal Disease ◽  
Growth Inhibition ◽  
Growth Regulation ◽  
Mesangial Cell ◽  
Growth Inhibitor ◽  
Puromycin Aminonucleoside ◽  
3T3 Fibroblasts ◽  
Growth Inhibitory Activity ◽  
Progressive Renal Disease

Mesangial cell proliferation is found in many forms of progressive renal disease. This proliferation may be due to dysregulation of mesangial cell growth. The studies presented here test the hypothesis that the normal glomerulus produces a regulator of mesangial cell growth. Conditioned media (CM) from primary glomerular cultures were able to inhibit rat mesangial cell growth in a dose- and time-dependent fashion, from 30.0 +/- 3.8 to 86.6 +/- 3.9% growth inhibition. The growth inhibitor in glomerular CM appears to have a molecular weight of less than 3,000. Glomerular CM caused significantly more growth inhibition than did 3T3 fibroblast CM, 77.9 +/- 2.8% growth inhibition by 10% glomerular CM versus 21.2 +/- 5.4% by 10% 3T3 CM (P < 0.001). The growth inhibition was completely reversible. Glomerular CM had no effect on the growth of 3T3 fibroblasts. Treatment of the glomerular CM with either trypsin or neutral protease had no effect on its growth inhibitory activity. Glomerular CM obtained from rats with puromycin aminonucleoside nephrosis caused significantly less growth inhibition than did control glomerular CM; at a concentration of 10% CM, control glomerular CM had 65.1 +/- 1.9% growth inhibition and puromycin had 45.4 +/- 2.1% (P < 0.001). Thus, the rat glomerulus produces a small, nonprotein inhibitor of rat mesangial cell growth and the activity of this inhibitor is reduced in puromycin nephrosis. Impairment of mesangial cell growth regulation may be important in the pathogenesis of progressive renal disease.

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