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Albumin-stimulated TGFbeta-1 in renal tubular cells is associated with activation of MAP kinase.

Abstract：

BACKGROUND:Proteinuric renal diseases are often associated with progressive tubulointerstitial fibrosis that usually defines the degree and rate of progression of renal failure. Glomerular filtration of excess albumin, the dominant protein in proteinuria, into proximal tubule could provide the stimulus to induce certain fibrogenic cytokines from proximal tubular cells (PTC), which may account for fibrosis in the interstitium. To explore this hypothesis we tested the effect of bovine albumin in PTC in culture on the expression and secretion of transforming growth factor (TGF) beta-1, a prominent fibrogenic cytokine. METHODS:TGFbeta-1 expressed by cultured PTC was measured by enzyme-linked immunosorbent assay (ELISA) and indirectly by reverse-transcription polymerase chain reaction (RT-PCR). Relative messenger ribonucleic acid (mRNA) levels were measured in ethidium bromides stained gels, by comparison to transcripts for 18s ribosomal RNA. Activated mitogen-activated protein (MAP) kinase was estimated by Western blot with phosphotyrosine-specific antibody. RESULTS:Following incubation of PTC with albumin determination of TGF beta-1 mRNA in PTC and TGF beta-protein in culture medium both indicated a time- and dose-dependent increase. MAP kinase (p44/42) was activated within 5 min of exposure to albumin. Inhibition of the MAP kinase cascade by PD98059 attenuated the effect of albumin on TGF beta-1 expression. CONCLUSIONS:These observations suggest that overexpression of TGF beta-1 by PTC in response to albumin is regulated through a MAP kinase signaling pathway. This mechanism may play a role in the development of interstitial fibrosis in proteinuric states.

journal_name

Int Urol Nephrol

journal_title

International urology and nephrology

authors

Zhao J,Tramontano A,Makker SP

doi

10.1007/s11255-007-9249-z

subject

Has Abstract

pub_date

2007-01-01 00:00:00

pages

1265-71

issue

4

eissn

0301-1623

issn

1573-2584

journal_volume

39

pub_type

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