Linkage between α1 Adrenergic Receptor and the Jak/STAT Signaling Pathway in Vascular Smooth Muscle Cells

• Published in: Biochemical and biophysical research communications 2000-02, Vol.268 (1), p.25-30
• Main Authors: Sasaguri, Toshiyuki, Teruya, Hiroshi, Ishida, Akio, Abumiya, Takeo, Ogata, Jun
• Format: Article
• Language: English
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.1999.2066

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 α1B 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.