RGD Reference Report - Activation of PI3-kinase/PKB contributes to delay in neutrophil apoptosis after thermal injury. - Rat Genome Database

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Activation of PI3-kinase/PKB contributes to delay in neutrophil apoptosis after thermal injury.

Authors: Hu, Z  Sayeed, MM 
Citation: Hu Z and Sayeed MM, Am J Physiol Cell Physiol. 2005 May;288(5):C1171-8. Epub 2004 Dec 29.
RGD ID: 2292697
Pubmed: PMID:15625305   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpcell.00312.2004   (Journal Full-text)

Neutrophil apoptosis is delayed under trauma and/or sepsis injury conditions. The molecular mechanism for the delay in apoptosis has not been well defined. We investigated whether activation of phosphatidyl inositol 3-kinase (PI3-kinase)/PKB signaling pathway contributes to the delay in neutrophil apoptosis with thermal injury. Rats were subjected to burns (30% total body surface area, 98 degrees C for 10 s), and euthanized 24 h later. Blood neutrophils were isolated with the use of Ficoll gradient centrifugation and cultured for the indicated time periods. Apoptosis was determined using annexin V and PI labeling and flow cytometry. NF-kappaB activation was examined using gel mobility shift assay and confocal microscopy. Expression levels of inhibitory apoptosis proteins (IAPs), including cellular IAP1 (cIAP1), cIAP2, X-linked IAP (XIAP), and survivin, and Bcl-2 family members such as Bcl-xl and Bad, were determined by Western blot analysis and/or RT-PCR, real-time PCR. The results showed that in culture, the decrease in apoptosis of neutrophils from thermally injured rats was prevented in the presence of PI3-kinase inhibitors wortmannin and LY-294002. There was upregulation of PKB and Bad phosphorylation and NF-kappaB activation in N-formyl-l-methionyl-l-leucyl-l-phenylalanine-stimulated neutrophils from thermally injured rats compared with the sham injured group. Increased Bad phosphorylation and NF-kappaB activation were also attenuated by wortmannin. Bcl-xl expression in neutrophils was upregulated with thermal injury and inhibited in the presence of wortmannin. However, the expression of IAP family members was neither affected by thermal injury nor inhibited by wortmannin. These data suggest that the delay in neutrophil apoptosis with thermal injury is partly caused by activation of PI3-kinase/PKB signaling and NF-kappaB, which appeared to be related to the increased Bcl-xl expression and phosphorylation of Bad, but not IAP expression.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
BADHumanBurns  ISOBad (Rattus norvegicus)protein:increased expression:neutrophilRGD 
BadRatBurns  IEP protein:increased expression:neutrophilRGD 
BadMouseBurns  ISOBad (Rattus norvegicus)protein:increased expression:neutrophilRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
BadRatresponse to wortmannin  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bad  (BCL2-associated agonist of cell death)

Genes (Mus musculus)
Bad  (BCL2-associated agonist of cell death)

Genes (Homo sapiens)
BAD  (BCL2 associated agonist of cell death)


Additional Information