A calpain-like protease inhibits autophagic cell death

Autophagy. 2007 Sep-Oct;3(5):519-22. doi: 10.4161/auto.4052. Epub 2007 Feb 23.

Abstract

Programmed cell death (PCD) plays critical roles during development and in disease states. One form of programmed cell death utilizes autophagy--a cellular mechanism of degrading bulk cytosolic components--to destroy cells. Previously, the broad-spectrum caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD) was shown to induce autophagic cell death. The mechanism of Zvad-induced cell death was proposed to require caspase-8 inhibition. In our report, we extend these findings to show that--as is the case for apoptosis--induction of autophagic cell death in response to zVAD results in phosphatidylserine exposure prior to loss of membrane integrity. Additionally, we show that caspase-8 inhibition is insufficient to cause autophagic cell death. Rather, the activity of a calpain-like protease must also be blocked. These results reveal the existence of an autophagic PCD-inhibiting calpain-like cysteine protease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Chloromethyl Ketones / pharmacology
  • Animals
  • Autophagy / drug effects*
  • Autophagy / physiology
  • Caspase 8
  • Caspase Inhibitors
  • Cell Line
  • Cysteine Proteinase Inhibitors / pharmacology
  • Mice
  • Phosphatidylserines / metabolism

Substances

  • Amino Acid Chloromethyl Ketones
  • Caspase Inhibitors
  • Cysteine Proteinase Inhibitors
  • Phosphatidylserines
  • benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
  • Casp8 protein, mouse
  • Caspase 8