In rat neonatal myocytes, a constitutively active Gαq causes cellular injury and apoptosis. However, stimulation of the α1-adrenergic receptor, one of the Gq protein-coupled receptors, with phenylephrine for 48 h causes little cellular injury and apoptosis. Expression of the Gβγ-sequestering peptide βARK-ct increases the phenylephrine-induced cardiac injury, indicating that Gβγ released from Gq counteracts the Gαq-mediated cellular injury. Stimulation with phenylephrine activates extracellular signal-regulated kinase (ERK) and Akt, and activation is significantly blunted by βARK-ct. Inhibition of Akt by inhibitors of phosphatidylinositol 3-kinase increases the cellular injury induced by phenylephrine stimulation. In contrast to the inhibition of Akt, inhibition of ERK does not affect the phenylephrine-induced cardiac injury. These results suggest that Gβγ released from Gq upon α1-adrenergic receptor stimulation activates ERK and Akt. However, activation of Akt but not ERK plays an important role in the protection against the Gαq-induced cellular injury and apoptosis.
|Number of pages||6|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Mar 8 2002|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology