Calpain inhibitor I decreases beta A4 secretion from human embryonal kidney cells expressing beta-amyloid precursor protein carrying the APP670/671 double mutation

Neurosci Lett. 1995 Dec 1;201(1):29-32. doi: 10.1016/0304-3940(95)12122-k.

Abstract

We have investigated the effects of the cell-penetrating cysteine protease inhibitors calpain inhibitor I (N-acetyl-Leu-Leu-norleucinal) and calpain inhibitor II (N-acetyl-Leu-Leu-methioninal) on the secretion of the beta-amyloid peptide (beta A4) using transiently transfected cells expressing beta-amyloid precursor protein (APP) with the NL670/671 double mutation. Calpain inhibitor I markedly reduced the amounts of immunoprecipitable beta A4 and p3 peptide released into the culture medium. Within the cells C-terminal APP fragments accumulated. Since beta A4 secretion by cells expressing the 100 amino acid long APP C-terminus was also reduced by calpain inhibitor I, we conclude that this substance directly or indirectly interferes with the gamma-secretase activity responsible for generating the beta A4 and p3 C-termini.

MeSH terms

  • Amino Acid Sequence
  • Amyloid beta-Peptides / biosynthesis
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Protein Precursor / biosynthesis*
  • Amyloid beta-Protein Precursor / genetics*
  • Cell Line
  • Cysteine Proteinase Inhibitors / pharmacology*
  • Glycoproteins / pharmacology*
  • Humans
  • Kidney / embryology
  • Kidney / metabolism*
  • Molecular Sequence Data
  • Mutation

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Cysteine Proteinase Inhibitors
  • Glycoproteins
  • amyloid beta-protein p3, human
  • calpain inhibitors