Involvement of metallo-endopeptidase in degradation of luteinizing hormone-releasing hormone by neuronal and glial cells cultured from rat fetal brain

Neuropeptides. 1991 Feb;18(2):77-82. doi: 10.1016/0143-4179(91)90004-3.

Abstract

Luteinizing hormone-releasing hormone (LHRH) was degraded by neuronal and glial cells cultured from fetal rat brain. The degradation of LHRH by neuronal cells was strongly inhibited by a metal chelator. Captopril only inhibited by generation of fragment (1-3) from fragment (1-5). In the presence of captopril, fragment (1-5) accumulated in the highest amount among the N-terminal fragments identified. The initial cleavage of LHRH, as determined by following the loss of the LHRH peak, was strongly inhibited by thiol-blocking reagents, as well as metal chelators. The results with glial cells were almost the same as those seen with neuronal cells. Thus, we propose that a thiol-dependent membrane-bound metallo-endopeptidase plays a major role in the initial stage of degradation of LHRH at the Tyr5-Gly6 bond in both neurons and glia. Angiotensin-converting enzyme is involved in the secondary process of the LHRH degradation in both cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Brain / enzymology*
  • Captopril / pharmacology
  • Cells, Cultured
  • Fetus
  • Gonadotropin-Releasing Hormone / metabolism*
  • Metalloendopeptidases / metabolism*
  • Molecular Sequence Data
  • Neuroglia / drug effects
  • Neuroglia / enzymology*
  • Neurons / drug effects
  • Neurons / enzymology*
  • Peptide Fragments / isolation & purification
  • Protease Inhibitors / pharmacology*
  • Rats

Substances

  • Peptide Fragments
  • Protease Inhibitors
  • Gonadotropin-Releasing Hormone
  • Captopril
  • Metalloendopeptidases