(Hypertension. 1996;27:465-475.)
© 1996 American Heart Association, Inc.
Articles |
Mechanisms for Inducible Control of Angiotensinogen Gene Transcription
From the Department of Internal Medicine and Sealy Center for Molecular Science, University of Texas Medical Branch, Galveston.
Correspondence to Allan R. Brasier, 3.142 Medical Research Building, 301 University Blvd, Galveston, TX 77555-1060. E-mail abrasier%intmeds1@mhost.utmb.edu.
Abstract The intravascular renin-angiotensin
system is an endocrine system designed to maintain
cardiovascular homeostasis in response to hypotension.
Under normal conditions, angiotensinogen concentrations
circulating in the plasma are rate limiting for the maximum velocity of
angiotensin I formation. In the liver, the major site of
circulating angiotensinogen synthesis,
angiotensinogen expression is under exquisite hormonal
control. We review the mechanisms by which hormones effect
transcriptional control of angiotensinogen expression.
Adrenal-derived glucocorticoids produce the translocation of the
glucocorticoid receptor into the nucleus. It in turn binds to two
glucocorticoid response elements and stimulates
angiotensinogen gene transcription. Inflammation
activates angiotensinogen transcription as a result
of the macrophage-derived cytokines
interleukin-1 and tumor necrosis factor-
. These cytokines
change the abundance of two transcription factor families that bind a
single regulatory site in the angiotensinogen promoter, the
acute-phase response element. These proteins include the nuclear
factor-
B complex and the CCAAT/enhancer binding protein family.
Activation of the renin-angiotensin system, through
production of angiotensin II, results in feedback
stimulation of angiotensinogen synthesis (the "positive
feedback loop"). We have discovered that the nuclear factor-B
transcription factor is regulated by angiotensin II, a
finding that provides a mechanism for the transcriptional component of
angiotensinogen gene synthesis in the positive feedback
loop. These studies underscore the concept that induction of the
angiotensinogen gene by diverse
physiological stimuli is mediated through changes
in the nuclear abundance of sequence-specific transcription
factors. The intracellular convergence of cytokine- and
angiotensin II–induced signaling pathways on the nuclear
factor-B transcription factor provides a point for "cross
talk" between angiotensin- and
cytokine-activated second messenger pathways.
Key Words: nuclear factor-B • angiotensinogen • nuclear factor-IL6
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