Interaction of neuronal nitric oxide synthase with alpha1-adrenergic receptor subtypes in transfected HEK-293 cells

BMC Pharmacol. 2002 Aug 16:2:17. doi: 10.1186/1471-2210-2-17.

Abstract

Background: The C-terminal four amino acids (GEEV) of human alpha1A-adrenergic receptors (ARs) have been reported to interact with the PDZ domain of neuronal nitric oxide synthase (nNOS) in a yeast two-hybrid system. The other two alpha1-AR subtypes have no sequence homology in this region, raising the possibility of subtype-specific protein-protein interactions.

Results: We used co-immunoprecipitation and functional approaches with epitope-tagged alpha1-ARs to examine this interaction and the importance of the C-terminal tail. Following co-transfection of HEK-293 cells with hexahistidine/Flag (HF)-tagged alpha1A-ARs and nNOS, membranes were solubilized and immunoprecipitated with anti-FLAG affinity resin or anti-nNOS antibodies. Immunoprecipitation of HFalpha1A-ARs resulted in co-immunoprecipitation of nNOS and vice versa, confirming that these proteins interact. However, nNOS also co-immunoprecipitated with HFalpha1B- and HFalpha1D-ARs, suggesting that the interaction is not specific to the alpha1A subtype. In addition, nNOS co-immunoprecipitated with each of the three HFalpha1-AR subtypes which had been C-terminally truncated, suggesting that this interaction does not require the C-tails; and with Flag-tagged beta1- and beta2-ARs. Treatment of PC12 cells expressing HFalpha1A-ARs with an inhibitor of nitric oxide formation did not alter norepinephrine-mediated activation of mitogen activated protein kinases, suggesting nNOS is not involved in this response.

Conclusions: These results show that nNOS does interact with full-length alpha1A-ARs, but that this interaction is not subtype-specific and does not require the C-terminal tail, raising questions about its functional significance.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies / pharmacology
  • Cells, Cultured
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Mitogen-Activated Protein Kinases / metabolism
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase / immunology
  • Nitric Oxide Synthase / metabolism*
  • Nitric Oxide Synthase Type I
  • PC12 Cells
  • Precipitin Tests
  • Protein Binding
  • Protein Structure, Tertiary / physiology*
  • Rats
  • Receptors, Adrenergic, alpha-1 / chemistry
  • Receptors, Adrenergic, alpha-1 / genetics
  • Receptors, Adrenergic, alpha-1 / metabolism*
  • Transfection

Substances

  • ADRA1A protein, human
  • ADRA1B protein, human
  • Adra1a protein, rat
  • Adra1b protein, rat
  • Antibodies
  • Enzyme Inhibitors
  • Receptors, Adrenergic, alpha-1
  • NOS1 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type I
  • Nos1 protein, rat
  • Mitogen-Activated Protein Kinases
  • NG-Nitroarginine Methyl Ester