TY - JOUR
T1 - Linkage between α1 adrenergic receptor and the Jak/STAT signaling pathway in vascular smooth muscle cells
AU - Sasaguri, Toshiyuki
AU - Teruya, Hiroshi
AU - Ishida, Akio
AU - Abumiya, Takeo
AU - Ogata, Jun
N1 - Funding Information:
This study was supported in part by grants from the Ministry of Education, Science, and Culture (a Grant-in-Aid for Scientific Re- search), the Ministry of Health and Welfare (Research Grants for Cardiovascular Diseases), Science and Technology Agency (Special Coordination Funds for Promoting Science and Technology [Encouragement System of COE]), and Japan Cardiovascular Research Foundation.
PY - 2000/2/5
Y1 - 2000/2/5
N2 - The Jak/STAT pathway is activated following stimulation of the type I angiotensin II receptor. To examine whether this pathway is shared among other G-protein-coupled receptors, we studied the linkage between the α1 adrenergic receptor and this pathway. The α1 agonist phenylephrine induced tyrosine phosphorylation of Jak2, Tyk2, and STAT1 in vascular smooth muscle cells. The phosphorylation of Jak2 was prevented by the α1 receptor antagonists prazosin and chloroethylclonidine, but not by WB4101, and that of STAT1 was inhibited by prazosin and the Jak2 inhibitor AG490. After stimulation with phenylephrine, Jak2 and STAT1 were found to associate with α(1B) receptor. Phenylephrine stimulated the DNA binding activity of STAT1. Protein synthesis promoted by phenylephrine was inhibited by prazosin, AG490, and the introduction of a decoy oligonucleotide for STAT1. These results suggested that α1 receptor is linked to the Jak/STAT pathway and that this pathway mediates α1 agonist-induced smooth muscle hypertrophy. (C) 2000 Academic Press.
AB - The Jak/STAT pathway is activated following stimulation of the type I angiotensin II receptor. To examine whether this pathway is shared among other G-protein-coupled receptors, we studied the linkage between the α1 adrenergic receptor and this pathway. The α1 agonist phenylephrine induced tyrosine phosphorylation of Jak2, Tyk2, and STAT1 in vascular smooth muscle cells. The phosphorylation of Jak2 was prevented by the α1 receptor antagonists prazosin and chloroethylclonidine, but not by WB4101, and that of STAT1 was inhibited by prazosin and the Jak2 inhibitor AG490. After stimulation with phenylephrine, Jak2 and STAT1 were found to associate with α(1B) receptor. Phenylephrine stimulated the DNA binding activity of STAT1. Protein synthesis promoted by phenylephrine was inhibited by prazosin, AG490, and the introduction of a decoy oligonucleotide for STAT1. These results suggested that α1 receptor is linked to the Jak/STAT pathway and that this pathway mediates α1 agonist-induced smooth muscle hypertrophy. (C) 2000 Academic Press.
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U2 - 10.1006/bbrc.1999.2066
DO - 10.1006/bbrc.1999.2066
M3 - Article
C2 - 10652206
AN - SCOPUS:0034607040
SN - 0006-291X
VL - 268
SP - 25
EP - 30
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -