(Hypertension. 1999;33:108-115.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Role of C/A Polymorphism at -20 on the Expression of Human Angiotensinogen Gene
Presented in part at the 69th Scientific Sessions of the American Heart Association, New Orleans, La, November 10–13, 1996, and published in abstract form (Circulation. 1996;94[pt 1]:4049.).
From the Department of Pathology, New York Medical College, Valhalla, NY.
Correspondence to Ashok Kumar, PhD, Room 455, Basic Science Building, New York Medical College, Valhalla, NY 10595. E-mail ashok_kumar{at}nymc.edu
Abstract—Angiotensinogen
is the glycoprotein precursor of 1 of the most potent
vasoactive hormones, angiotensin II. Human
angiotensinogen gene contains a C/A polymorphism
at -20 located between the TATA box and transcriptional initiation
site. We show here that when nucleoside A is present at -20, this
sequence binds to the estrogen receptor. We also show that
transcriptional activity of reporter constructs containing human
angiotensinogen gene promoter with nucleoside A at -20 is
increased on cotransfection of an expression vector containing human
estrogen receptor-
coding sequence in human hepatoma cells (HepG2)
followed by estrogen treatment. On the other hand, adenoviral major
late transcription factor binds preferentially to this region of the
promoter when nucleoside C is present at -20. We also show that
reporter constructs containing human angiotensinogen gene
promoter with nucleoside C at -20 have increased basal promoter
activity on transient transfection in HepG2 cells as compared with
reporter constructs with nucleoside A at -20. Our data suggest that
C/A polymorphism at -20 may modulate the expression of human
angiotensinogen gene in a sex-specific manner.
Key Words: angiotensinogen • genes • polymorphism • estrogen • gene regulation • regulation, hormonal • major late transcription factor
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