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Papers In Press, published online ahead of print October 16, 2003
Physiology Dept., Regensburg University, Regensburg 93053
Corresponding Author: vladimir.todorov{at}vkl.uni-regensburg.de
TNF
J. Biol. Chem, 10.1074/jbc.M308697200
Submitted on August 6, 2003
Revised on October 14, 2003
Accepted on October 16, 2003
TNF
activates NFkB to inhibit renin transcription by targeting cAMP responsive element
is known to inhibit renin gene expression in juxtaglomerular (JG) cells, which are the main source of renin in vivo. In the present study we aimed to characterize the intracellular mechanisms of TNF signaling to renin gene in the mouse JG cell line As4.1. TNF was found to activate nuclear factor NFkB, which is one of the principal intracellular mediators of TNF signal transduction. Constitutive activation of NFkB suppressed renin gene transcription, but NFkB appeared not to target the NFkB binding sites in the renin promoter. Thus, NFkB, but not the canonical NFkB binding sequences in the renin promoter, seemed to be involved in the suppression of renin transcription by TNF. Deletion/mutation analysis revealed that the effect of TNF on renin gene is transmitted by a cAMP Responsive Element (CRE) located at -2697 to -2690. Mobility shift/supershift assays evidenced for the presence of NFkB proteins in the complex that binds to mouse renin CRE. Our results strongly suggest that NFkB mediates the effect of TNF on renin transcription targeting a CRE in the mouse renin promoter.
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