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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00142.2002
Submitted on March 1, 2002
Accepted on June 25, 2002
* To whom correspondence should be addressed. E-mail: vladimir.todorov{at}vkl.uni-regensburg.de.
Renin, produced in renal juxtaglomerular (JG) cells, is a fundamental regulator of blood pressure. Accumulating evidence suggests that cytokines may influence directly renin production in the JG cells. Tumor necrosis factor alpha (TNFalpha), which is one of the key mediators in immunity and inflammation, is known to participate in the control of vascular proliferation and contraction, and hence in the pathogenesis of cardiovascular diseases. Thus, TNFalpha may exert its effects upon the cardiovascular system, through modulation of renal renin synthesis. Therefore we have tested the effect of TNFalpha on renin transcription in As4.1 cells, which represent transformed mouse JG cells, and in native mouse JG cells in culture. Renin gene expression was also determined in mice lacking the gene for TNFalpha (TNFalpha knockout mice). TNFalpha inhibited renin gene expression via an inhibition of the transcriptional activity, targeting the proximal 4.1 kb of the renin promoter in As4.1 cells. TNFalpha also attenuated forskolin stimulated renin gene expression in primary cultures of mouse JG cells. Mice lacking the TNFalpha gene had almost 3-fold higher basal renal renin mRNA abundance relative to the control strain. The general physiological regulation of renin expression by salt was not disturbed in TNFalpha knockout mice. Our data suggest that TNFalpha inhibits renin gene transcription at the cellular level and thus may act as a modulator of renin synthesis in (physio)pathological situations.
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