Mice deficient for the lysosomal proteinase cathepsin D exhibit progressive atrophy of the intestinal mucosa and profound destruction of lymphoid cells

EMBO J. 1995 Aug 1;14(15):3599-608. doi: 10.1002/j.1460-2075.1995.tb00029.x.

Abstract

Mice deficient for the major lysosomal aspartic proteinase cathepsin D, generated by gene targeting, develop normally during the first 2 weeks, stop thriving in the third week and die in a state of anorexia at day 26 +/- 1. An atrophy of the ileal mucosa first observed in the third week progresses towards widespread intestinal necroses accompanied by thromboemboli. Thymus and spleen undergo massive destruction with fulminant loss of T and B cells. Lysosomal bulk proteolysis is maintained. These results suggest, that vital functions of cathepsin D are exerted by limited proteolysis of proteins regulating cell growth and/or tissue homeostasis, while its contribution to bulk proteolysis in lysosomes appears to be non-critical.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Atrophy
  • B-Lymphocytes / pathology
  • Cathepsin D / antagonists & inhibitors
  • Cathepsin D / biosynthesis
  • Cathepsin D / deficiency*
  • Cathepsin D / genetics
  • Chimera
  • Fibroblasts / metabolism
  • Gene Targeting
  • Ileum / pathology
  • Intestinal Mucosa / pathology*
  • Leupeptins / pharmacology
  • Lysosomes / enzymology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Pepstatins / pharmacology
  • RNA, Messenger / biosynthesis
  • Specific Pathogen-Free Organisms
  • Spleen / pathology*
  • T-Lymphocytes / pathology
  • Thymus Gland / pathology*

Substances

  • Leupeptins
  • Pepstatins
  • RNA, Messenger
  • Streptomyces pepsin inhibitor
  • Cathepsin D
  • leupeptin
  • pepstatin