© 1999 American Heart Association, Inc.
Original Contribution |
Angiotensin II Induces Interleukin-6 Transcription in Vascular Smooth Muscle Cells Through Pleiotropic Activation of Nuclear Factor-
B Transcription Factors
From the Department of Internal Medicine (Y.H.), Sealy Center for Molecular Cardiology (M.S.R.), and Sealy Center for Molecular Science (A.R.B.), University of Texas Medical Branch, Galveston, Tex.
Correspondence to Allan R. Brasier, Division of Endocrinology, MRB 8.138, University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555-1060. E-mail arbrasie{at}utmb.edu
Abstract—Interleukin-6
(IL-6) is a multifunctional cytokine expressed by
angiotensin II (Ang II)-stimulated vascular smooth muscle
cells (VSMCs) that functions as an autocrine growth factor. In this
study, we analyze the mechanism for Ang II-inducible IL-6
expression in quiescent rat VSMCs. Stimulation with the Ang II agonist
Sar1 Ang II (100 nmol/L) induced transcriptional expression
of IL-6 mRNA transcripts of 1.8 and 2.4 kb. In transient transfection
assays of IL-6 promoter/luciferase reporter plasmids, Sar1
Ang II treatment induced IL-6 transcription in a manner completely
dependent on the nuclear factor-
B (NF-B) motif. Sar1
Ang II induced cytoplasmic-to-nuclear translocation of the NF-B
subunits Rel A and NF-B1 with parallel changes in DNA-binding
activity in a biphasic manner, which produced an early peak at 15
minutes followed by a nadir 1 to 6 hours later and a later peak at 24
hours. The early phase of NF-B translocation was dependent on weak
simultaneous proteolysis of the IB
and ß
inhibitors, whereas later translocation was associated with
enhanced processing of the p105 precursor into the mature 50-kDa
NF-B1 form. Pretreatment with a potent inhibitor of
IB proteolysis, TPCK, completely blocked Sar1 Ang
IIAng II-induced NF-B activation and induction of
endogenous IL-6 gene expression, which indicated the
essential role of NF-B in mediating IL-6 expression. We conclude
that Ang II is a pleiotropic regulator of the NF-B transcription
factor family and may be responsible for activating the expression of
cytokine gene networks in VSMCs.
Key Words: nuclear factor-B • renin-angiotensin system • angiotensin II • cytokine
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