An antibody against a CFTR-derived synthetic peptide, incorporated into living submandibular cells, inhibits beta-adrenergic stimulation of mucin secretion

Biochem Biophys Res Commun. 1992 Nov 16;188(3):1146-52. doi: 10.1016/0006-291x(92)91351-p.

Abstract

An antibody raised against a peptide in the first nucleotide-binding domain (NBD) of CFTR [1], incorporated into intact rat submandibular acini by hypotonic swelling, inhibited beta-adrenergic stimulated mucin secretion, without affecting cyclic AMP rise. The data are the first to show that a CFTR-antibody-containing cell results in defective stimulation of mucin secretion, as is seen in CF cells, and that this can be reversed by an excessive increase in cyclic AMP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Adenosine Triphosphate / analysis
  • Adrenergic beta-Agonists / pharmacology*
  • Animals
  • Antibodies / pharmacology*
  • Cyclic AMP / analogs & derivatives
  • Cyclic AMP / analysis
  • Cyclic AMP / pharmacology
  • Cystic Fibrosis / metabolism*
  • Cystic Fibrosis Transmembrane Conductance Regulator
  • Dose-Response Relationship, Drug
  • Humans
  • Isoproterenol / pharmacology
  • Membrane Proteins / immunology*
  • Mucins / metabolism*
  • Peptide Fragments / immunology
  • Rats
  • Submandibular Gland / cytology
  • Submandibular Gland / drug effects*
  • Thionucleotides / pharmacology

Substances

  • Adrenergic beta-Agonists
  • Antibodies
  • CFTR protein, human
  • Membrane Proteins
  • Mucins
  • Peptide Fragments
  • Thionucleotides
  • Cystic Fibrosis Transmembrane Conductance Regulator
  • 8-((4-chlorophenyl)thio)cyclic-3',5'-AMP
  • Adenosine Triphosphate
  • Cyclic AMP
  • Isoproterenol
  • 1-Methyl-3-isobutylxanthine