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- W2282770832 abstract "Neutrophils (PMNs) are short-lived cells that constitutively undergo apoptosis to prevent excessive tissue damage. We previously identified NF-E2 as an Akt substrate in human PMNs, and showed that antibody depletion of NF-E2 delayed PMN apoptosis at 24 hours as assessed by propidium iodide flow cytometry. Additionally, NF-E2 depletion of PMNs increased IκB phosphorylation, a marker of NFκB activation with concomitant increases in pro-survival Mcl-1 expression. These studies led us to hypothesize that NF-E2 promotes constitutive PMN apoptosis by inhibiting NFκB activation. Preliminary EMSA revealed increased PMN NFκB DNA binding after NF-E2 depletion. Furthermore, co-transfection of HEK-293 cells with NF-E2 and NFκB luciferase reporter resulted in significantly lower NFκB luciferase promoter activity after TNF-α stimulation as compared to vector and NFκB luciferase reporter transfected cells. These results collectively demonstrate that NF-E2 regulates PMN apoptosis by inhibiting NFκB activity. In our future studies, we will utilize NFκB inhibitors to further delineate a role for NFκB in promoting PMN survival and Mcl-1 expression as a consequence of NF-E2 depletion. Taken together, our results suggest that NF-E2 is a pro-apoptotic protein that promotes constitutive PMN apoptosis by inhibiting NFκB-mediated transcription of pro-survival genes. Support for this work was provided by AHA #0815433D (PRJ) and AHA #0335278N, NIH/NIAID #1R56AI059165-01A2, RO1AI075212-01A1 (MJR). ASBMMB abstract, EB2009, Deadline November 5, 2008" @default.
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- W2282770832 date "2009-04-01" @default.
- W2282770832 modified "2023-10-15" @default.
- W2282770832 title "Nuclear factor erythroid derived‐2 (NF‐E2)‐mediated regulation of NF‐kB activation in neutrophils: A potential mechanism of NF‐E2‐mediated apoptosis" @default.
- W2282770832 doi "https://doi.org/10.1096/fasebj.23.1_supplement.526.6" @default.
- W2282770832 hasPublicationYear "2009" @default.
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