Ephedrine induced Thioredoxin-1 expression through β-adrenergic receptors/Cyclic AMP/protein kinase A/dopamine- and Cyclic AMP-regulated phosphoprotein signaling pathway.

In this study, we found that Eph induced Trx-1 expression, which was inhibited by propranolol (β-adrenergic receptors inhibitor), but not by phenoxybenzamine (α-adrenergic receptors inhibitor) in rat pheochromocytoma PC12 cells. Moreover, the increase of Trx-1 expression was inhibited by SQ22536 (adenylyl cyclase inhibitor) and H-89 (protein kinase A inhibitor). Interestingly, the effect of Eph on dopamine- and Cyclic AMP-regulated phosphoprotein (DARPP-32) was similar to Trx-1. Thus, the relationship between Trx-1 and DARPP-32 was further studied. The DARPP-32 siRNA significantly reduced Trx-1 expression, but Trx-1 siRNA did not exchange DARPP-32. These results suggested that Eph induced the Trx-1 expression through β-adrenergic receptors/Cyclic AMP/PKA/DARPP-32 signaling pathway. Furthermore, Eph induced PKA-mediated Cyclic AMP response element-binding protein (CREB) phosphorylation. Down-regulation of DARPP-32 expression decreased phosphorylated CREB. In addition, Eph had a significant effect on the viability of the rat pheochromocytoma PC12 cells through β-adrenergic receptors. Trx-1 may play an important role in the actions of Eph. PMID: 23416460 [PubMed - as supplied by publisher]
Source: Cellular Signalling - Category: Cytology Authors: Tags: Cell Signal Source Type: research