GATA-3 is upregulated in peripheral blood mononuclear cells from patients with minimal change nephrotic syndrome

2009 ◽  
Vol 71 (06) ◽  
pp. 608-616 ◽  
Author(s):  
A. Komatsuda ◽  
H. Wakui ◽  
K. Iwamoto ◽  
M. Togashi ◽  
R. Masai ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Transcriptional and Post-Transcriptional Alterations of I κBα in Active Minimal-Change Nephrotic Syndrome

2001 ◽  
Vol 12 (8) ◽  
pp. 1648-1658 ◽  
Author(s):  
DJILLALI SAHALI ◽  
ANDRÉ PAWLAK ◽  
SABINE LE GOUVELLO ◽  
PHILIPPE LANG ◽  
ASTA VALANCIUTÉ ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Minimal Change Nephrotic Syndrome ◽  
Binding Activity ◽  
Minimal Change ◽  
Peripheral Blood Mononuclear ◽  
Nuclear Extracts ◽  
Blood Mononuclear Cells

Abstract. Minimal-change nephrotic syndrome (MCNS) is a renal disease characterized by heavy glomerular proteinuria and increased production of cytokines by immune cells. Because of the central role of nuclear factor-κB (NF-κB) in the regulation of cytokine expression, its activity during the relapse and remission phases of steroid-sensitive MCNS was analyzed. During relapse, nuclear extracts from peripheral blood mononuclear cells displayed high levels of NF-κB DNA-binding activity, consisting primarily of p50/RelA (p65) complexes. NF-κB p65 and IκBα proteins were barely detected or not detected in cytosolic fractions during relapse, in contrast to remission. The lack of expression of IκBα protein was associated with downregulation of IκBα mRNA and increases in the levels of the mRNA encoding the proteasome α2 subunit proteolytic pathway. In addition, inhibition of proteasome activity induced cytosolic accumulation of phosphorylated IκBα and significant reductions in the NF-κB binding activity in nuclear extracts from peripheral blood mononuclear cells from patients experiencing relapses. These results suggest that alterations in the NF-κB/IκBα regulatory feedback loop may contribute to the immunologic abnormalities that occur in steroidsensitive MCNS.

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