![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
I Duque, M Rodriguez Puyol, P Ruiz, M Gonzalez-Rubio, ML Diez Marques and D Rodriguez Puyol
Department of Physiology and Pharmacology, Alcala de Henares University, Madrid, Spain.
The present experiments were designed to assess a possible role of H2O2 in the proliferation of cultured rat mesangial cells, as well as to evaluate the effect of different calcium channel blockers and a platelet-activating factor antagonist on this proliferation. Cultured rat mesangial cells were plated at two densities (10,000 and 25,000 cells/well) in 24-well dishes, and proliferation was measured by analyzing [3H]thymidine incorporation and by directly counting the cells. Hydrogen peroxide, 100 microM, increased [3H]thymidine incorporation at the two densities tested (85 and 59%, respectively), as well as the number of cells (53 and 23%, respectively). This effect was dose dependent and it was blocked completely by verapamil and diltiazem, 10 microM, but not by TMB-8 [3,4,5-trimethoxybenzoic acid 8- (diethylamino) octyl ester] at the same concentration. BN 52021, a competitive antagonist of platelet-activating factor, only slightly blocked the H2O2-dependent proliferation. The inhibitory action of the two calcium antagonists tested started at concentrations as low as 1 nM, and inhibited completely the H2O2 stimulated proliferation at concentrations between 0.1 and 1 microM. These results establish that H2O2 is able to induce proliferation of mesangial cells. Although the pathophysiological implications of this finding remain to be proven, these data suggest a potential therapeutic action of calcium antagonist in inflammatory conditions such as glomerulonephritis.
This article has been cited by other articles:
|
|
 |
|
  N. R. Madamanchi, S. Li, C. Patterson, and M. S. Runge Reactive Oxygen Species Regulate Heat-Shock Protein 70 via the JAK/STAT Pathway Arterioscler. Thromb. Vasc. Biol., March 1, 2001; 21(3): 321 - 326. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Torrecillas, M. d. C. Boyano-Adánez, J. Medina, T. Parra, M. Griera, S. López-Ongil, E. Arilla, M. Rodríguez-Puyol, and D. Rodríguez-Puyol The Role of Hydrogen Peroxide in the Contractile Response to Angiotensin II Mol. Pharmacol., January 1, 2001; 59(1): 104 - 112. [Abstract] [Full Text]
|
|
|
|
 |
|
 C. I.-D. L. Cruz, P. Ruiz-Torres, R. G. del Moral, M. Rodriguez-Puyol, and D. Rodriguez-Puyol Age-related progressive renal fibrosis in rats and its prevention with ACE inhibitors and taurine Am J Physiol Renal Physiol, January 1, 2000; 278(1): F122 - F129. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. N. Rao, K. A. Katki, N. R. Madamanchi, Y. Wu, and M. J. Birrer JunB Forms the Majority of the AP-1 Complex and Is a Target for Redox Regulation by Receptor Tyrosine Kinase and G Protein-coupled Receptor Agonists in Smooth Muscle Cells J. Biol. Chem., February 26, 1999; 274(9): 6003 - 6010. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J P Grande Mechanisms of progression of renal damage in lupus nephritis:Pathogenesis of renal scarring Lupus, November 1, 1998; 7(9): 604 - 610. [Abstract] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
