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Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival.

Authors: Lamkanfi, M  Moreira, LO  Makena, P  Spierings, DC  Boyd, K  Murray, PJ  Green, DR  Kanneganti, TD 
Citation: Lamkanfi M, etal., Blood. 2009 Mar 19;113(12):2742-5. Epub 2009 Jan 23.
Pubmed: (View Article at PubMed) PMID:19168786
DOI: Full-text: DOI:10.1182/blood-2008-09-178038

Extensive apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linked to the excessive mortality associated with these disorders. Caspase inhibitors confer protection from endotoxin-induced lymphocyte apoptosis and improve survival, but it is not clear which caspases mediate lipopolysaccharide (LPS)-induced lymphocyte apoptosis and mortality. We report here that the apoptotic executioner caspase-7 was activated in the splenocytes of LPS-injected mice, suggesting a role for caspase-7 in lymphocyte apoptosis. Indeed, caspase-7-deficient mice were resistant to LPS-induced lymphocyte apoptosis and were markedly protected from LPS-induced lethality independently of the excessive production of serum cytokines. These results reveal for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by which caspase inhibitors protect from endotoxin-induced mortality.

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RGD Object Information
RGD ID: 5684539
Created: 2011-12-21
Species: All species
Last Modified: 2011-12-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.