Table 1

PARP deletion differentiates necrosis and apoptosis

TissueInsultsPathophysiologyRefs.
Necrosis associated: PARP−/− protects
In vivo models
MCAoCerebral ischemia9, 10
STZDiabetic damage12–14
ZymosanInflammation of multiple organs32
LAD-IRMyocardial ischemia11
TNBSInflammation of colon31
In vitro models
  CerebellumNMDA, SNP, SIN-1, OGDNecrosis9
  ThymocytesONOO, H2O2Necrosis40
  Islet cellsX/XONecrosis41
Apoptosis: PARP−/− does not protect
In vitro models
  CerebellumLow K+, STA, MPP+, ONOO, ColchicineApoptosis16
  ThymocytesEtoposide, DEX, Ceramide, IonomycinApoptosis16
  Hepatocytesα-CD95, ActD + TNFApoptosis16
  Bone marrowMNU, CPT-11, -IL-3Apoptosis42
  SplenocytesMNUApoptosis17
  Fibroblastsα-CD95 + CHX, MMSApoptosis42
  • MCAo, middle cerebral artery occlusion; NMDA, N-methyl-d-aspartate; SNP, sodium nitroprusside; SIN-1, 3-morpholino-sydnonimine hydrochloride; OGD, oxygen-glucose deprivation; STA, staurosporine; X/XO, hypoxanthine/xanthine oxidase; TNBS, trinitrobenzenesulfonic acid; STZ, streptozocin; MPP+, 1-methyl-4-phenylpyridinium; DEX, dexamethasone; ActD, actinomycin D; MNU, methylnitrosourea; CPT-11, a semisynthetic camptothecin derivative; MMS, N-methylmethanesulfonate; TNF, tumor necrosis factor; LAD-IR, ischemia and reperfusion of the left anterior descending coronary artery.