TY - JOUR
T1 - Angiotensin II can regulate gene expression by the AP-1 binding sequence via a protein kinase C-dependent pathway
AU - Takeuchi, Kazuhisa
AU - Nakamura, Norifumi
AU - Cook, Nigel S.
AU - Pratt, Richard E.
AU - Dzau, Victor J.
N1 - Funding Information:
This work was supported in part by NIH grants HL35610, HL35792, HL19259, HL35252, HL43131, HL42663. Dr. Takeuchi is the recipient of a JapanH eart Foundation Fellowship.
PY - 1990/11/15
Y1 - 1990/11/15
N2 - An expression vector containing three copies of the AP-1 binding element (TRE) upsteam of a thymidine kinase promotor which controlled the expression of the chloramphenicol acetyl transferase (CAT) gene was transiently transfected into vascular smooth muscle (VSM) cells and a human hepatocarcinoma cell line, Hep G2. Twelve hours of angiotensin (Ang) II exposure stimulated significantly CAT expression by 3.4 fold and 2.7 fold in Hep G2 and VSM cells, respectively. AngII had no effect on CAT expression of a control vector. This AngII-induced stimulation was attenuated significantly by an AngII receptor antagonist, Sar1Ile8 AngII, and abolished completely by a PKC inhibitor, staurosporine. Our data suggest that the TRE plays a crucial role in AngII-induced gene expression that is mediated by PKC. We concluded that TRE is one of the AngII-responsive elements.
AB - An expression vector containing three copies of the AP-1 binding element (TRE) upsteam of a thymidine kinase promotor which controlled the expression of the chloramphenicol acetyl transferase (CAT) gene was transiently transfected into vascular smooth muscle (VSM) cells and a human hepatocarcinoma cell line, Hep G2. Twelve hours of angiotensin (Ang) II exposure stimulated significantly CAT expression by 3.4 fold and 2.7 fold in Hep G2 and VSM cells, respectively. AngII had no effect on CAT expression of a control vector. This AngII-induced stimulation was attenuated significantly by an AngII receptor antagonist, Sar1Ile8 AngII, and abolished completely by a PKC inhibitor, staurosporine. Our data suggest that the TRE plays a crucial role in AngII-induced gene expression that is mediated by PKC. We concluded that TRE is one of the AngII-responsive elements.
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U2 - 10.1016/0006-291X(90)91574-C
DO - 10.1016/0006-291X(90)91574-C
M3 - Article
C2 - 2244902
AN - SCOPUS:0025223229
VL - 172
SP - 1189
EP - 1194
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -