AT(1) receptor Gαq protein-independent signalling transcriptionally activates only a few genes directly, but robustly potentiates gene regulation from the β2-adrenergic receptor

Mol Cell Endocrinol. 2011 Jan 1;331(1):49-56. doi: 10.1016/j.mce.2010.08.004. Epub 2010 Aug 12.

Abstract

The angiotensin II type 1 receptor (AT(1)R) is known to signal through heterotrimeric G proteins, and Gαq protein-independent signalling has only recently gained appreciation for profound impact on a diverse range of biological functions. β-Arrestins, among other central mediators of Gαq protein-independent signalling from the AT(1)R interact with transcriptional regulators and promote phosphorylation of nuclear proteins. However, the relative contribution of Gαq protein-independent signalling in AT(1)R mediated transcriptional regulation remains elusive. We here present a comprehensive comparative analysis of Gαq protein-dependent and -independent regulation of AT(1)R mediated gene expression. We found angiotensin II to regulate 212 genes, whereas Gαq-independent signalling obtained with the biased agonist, SII angiotensin II only regulated few genes. Interestingly, SII angiotensin II, like Ang II vastly potentiated β2-adrenergic receptor-stimulated gene expression. These novel findings indicate that the Gαq protein-independent signalling mainly modifies the transcriptional response governed by other signalling pathways, while direct induction of gene expression by the AT(1)R is dependent on classical Gαq protein activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology
  • GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism
  • Gene Expression Regulation* / drug effects
  • HEK293 Cells
  • Humans
  • Polymerase Chain Reaction
  • Receptor, Angiotensin, Type 1 / genetics
  • Receptor, Angiotensin, Type 1 / metabolism*
  • Receptors, Adrenergic, beta-2 / metabolism*
  • Reproducibility of Results
  • Response Elements / genetics
  • Signal Transduction / genetics*
  • Time Factors
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcription, Genetic* / drug effects

Substances

  • Receptor, Angiotensin, Type 1
  • Receptors, Adrenergic, beta-2
  • Transcription Factors
  • Angiotensin II
  • GTP-Binding Protein alpha Subunits, Gq-G11