G protein-coupled receptor kinases promote phosphorylation and beta-arrestin-mediated internalization of CCR5 homo- and hetero-oligomers

J Biol Chem. 2005 Nov 11;280(45):37503-15. doi: 10.1074/jbc.M500535200. Epub 2005 Sep 6.

Abstract

Expression levels of the chemokine receptor, CC chemokine receptor 5 (CCR5), at the cell surface determine cell susceptibility to HIV entry and infection. Cellular activation by CCR5 itself, but also by unrelated receptors leads to cross-phosphorylation and cross-internalization of CCR5. This study addresses the underlying molecular mechanisms of homologous and heterologous CCR5 regulation. As shown by bioluminescence resonance energy transfer experiments, CCR5 formed constitutive homo- as well as heterooligomeric complexes together with C5aR but not with the unrelated AT(1a)R in living cells. Stimulation with CCL5 of RBL cells, which co-expressed CCR5 together with an N-terminally truncated CCR5-DeltaNT mutant, resulted in both protein kinase C (PKC)- and G protein-coupled receptor (GPCR) kinase (GRK)-mediated cross-phosphorylation of the mutant unligated receptor, as determined by phosphosite-specific monoclonal antibody. Similarly, both PKC and GRK cross-phosphorylated CCR5 in a heterologous manner after C5a stimulation of RBL-CCR5/C5aR cells, whereas AT(1a)R stimulation resulted only in classical PKC-mediated CCR5 phosphorylation. Co-expression of CCR5-DeltaNT together with a phosphorylation-deficient CCR5 mutant that neither binds beta-arrestin nor undergoes internalization partially restored the CCL5-induced association of beta-arrestin with the homo-oligomeric receptor complex and augmented cellular uptake of (125)I-CCL5. Co-expression of C5aR, but not of AT(1a)R, promoted CCR5 co-internalization upon agonist stimulation by a mechanism independent of CCR5 phosphorylation. Co-internalization of phosphorylated CCR5 was also observed in C5a-stimulated macrophages. Finally, co-expression of a constitutively internalized C5aR-US28(CT) mutant led to intracellular accumulation of CCR5 in the absence of ligand stimulation. These results show that GRKs and beta-arrestin are involved in heterologous receptor regulation by cross-phosphorylating and co-internalizing unligated receptors within homo- or hetero-oligomeric protein complexes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arrestins / metabolism*
  • Cells, Cultured
  • Dimerization
  • Endocytosis*
  • Gene Expression Regulation
  • Humans
  • Macrophages / metabolism
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mutation
  • Phosphorylation
  • Protein Binding
  • Protein Kinase C / genetics
  • Protein Kinase C / metabolism
  • Protein Transport
  • Rats
  • Receptor, Anaphylatoxin C5a
  • Receptors, CCR5 / chemistry*
  • Receptors, CCR5 / genetics
  • Receptors, CCR5 / metabolism*
  • Receptors, Complement / genetics
  • Receptors, Complement / metabolism
  • Receptors, G-Protein-Coupled / metabolism*
  • beta-Arrestins

Substances

  • Arrestins
  • C5AR1 protein, human
  • Membrane Proteins
  • Receptor, Anaphylatoxin C5a
  • Receptors, CCR5
  • Receptors, Complement
  • Receptors, G-Protein-Coupled
  • beta-Arrestins
  • Protein Kinase C