Glycosylation-dependent binding of pancreatic type I phospholipase A2 to its specific receptor

Biochem Biophys Res Commun. 1995 Apr 6;209(1):293-9. doi: 10.1006/bbrc.1995.1502.

Abstract

Pancreatic group I phospholipase A2 (PLA2-I) elicits various biological responses via its specific receptor. The PLA2-I binding to its recombinant soluble receptor was considerably reduced after Peptide: N-glycosidase F treatment of the receptor. In cultured bovine smooth muscle cells, treatment with tunicamycin, a N-glycosylation inhibitor, resulted in a decrease in the number of PLA2-I receptor. In addition, the PLA2-I binding was blocked by the addition of a lectin, Wheat germ agglutinin. These results suggest an involvement of N-linked oligosaccharides of the PLA2-I receptor for its ligand recognition.

MeSH terms

  • Animals
  • Aorta / cytology
  • Aorta / metabolism
  • Cattle
  • Cells, Cultured
  • Glycosylation
  • Lectins / metabolism
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / metabolism
  • Pancreas / enzymology*
  • Phospholipases A / metabolism*
  • Phospholipases A2
  • Receptors, Cell Surface / drug effects
  • Receptors, Cell Surface / metabolism*
  • Receptors, Phospholipase A2
  • Substrate Specificity
  • Tunicamycin / pharmacology

Substances

  • Lectins
  • Receptors, Cell Surface
  • Receptors, Phospholipase A2
  • Tunicamycin
  • Phospholipases A
  • Phospholipases A2