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  • Title: Flice inhibitory protein is associated with the survival of neonatal neutrophils.
    Author: Rashmi R, Schnulle PM, Maddox AC, Armbrecht ES, Koenig JM.
    Journal: Pediatr Res; 2011 Oct; 70(4):327-31. PubMed ID: 21691254.
    Abstract:
    Neonatal polymorphonuclear leukocytes (PMN) exhibit delayed apoptosis both constitutively and under inflammatory conditions, and evidence has linked PMN longevity to the presence of antiapoptotic proteins. Activation of the survival-associated transcription factor, nuclear factor kappa B (NF-κB), promotes the synthesis of several antiapoptotic proteins including Flice inhibitory protein (FLIP). Neonatal and adult PMN were compared in this study to test the hypothesis that FLIP modulates age-related apoptosis. Expression of the short isoform, FLIP-S, was prominent at baseline and persisted during spontaneous apoptosis in neonatal PMN, whereas basal expression was lower and decreased under the same conditions in adult PMN. Stable FLIP-S expression in neonatal PMN was associated with a relative resistance to apoptosis in response to the protein synthesis inhibitor, cycloheximide (CHX), or the NF-κB inhibitor, gliotoxin. In contrast, similar treatment of adult PMN promoted greater overall apoptosis accompanied by FLIP degradation. Nuclear levels of phosphorylated p65, a critical NF-κB dimer, were relatively robust in neonatal PMN under basal conditions or after stimulation with TNF-α, a cytokine that induces FLIP. In conclusion, persistent FLIP-S expression is involved in the longevity of neonatal PMN, and our data suggest a contribution of NF-κB signaling and related survival mechanisms.
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