Expression of c-FLIP in a rat model of sepsis and its effects on endothelial apoptosis.

Mol Med Rep

Department of Intensive Care Unit, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.

Published: July 2017

AI Article Synopsis

  • Sepsis involves disrupted inflammatory responses, where apoptosis plays a key role in its development.
  • A study investigated c-FLIP, a protein that affects apoptosis signaling, in a rat model of sepsis, revealing lower levels of c-FLIPL in critical organs compared to controls.
  • The findings indicated that higher c-FLIPL levels correlate with decreased endothelial cell apoptosis, suggesting c-FLIP's potential significance in sepsis treatment strategies.

Article Abstract

Sepsis is characterized by the impaired regulation of inflammatory responses. Apoptosis is important in the pathogenesis of sepsis. Cellular FLICE‑inhibitory protein (c‑FLIP) is a catalytically inactive caspase‑8 homologue, which negatively interferes with apoptotic signaling. The role of c‑FLIP in sepsis and in endothelial cell apoptosis, a critical step in the pathogenesis of sepsis, remains controversial. In the present study, to investigate the relationship between c‑FLIP and sepsis, a rat model of sepsis was induced by cecal ligation and puncture, and western blot analysis was used to detect the expression of c‑FLIPL, the long isoform of c‑FLIP. Lower protein expression levels of c‑FLIPL were found in the brain, intestine and lung of the rat sepsis model, compared with the rats in the sham surgery group. The association between the expression of c‑FLIPL and endothelial cell apoptosis was further examined in vitro by c‑FLIPL overexpression and flow cytometry, which demonstrated that the expression of c‑FLIPL was inversely correlated with endothelial cell apoptosis. These data suggested that c‑FLIP may be important in sepsis and shed light on therapeutic strategies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482130PMC
http://dx.doi.org/10.3892/mmr.2017.6564DOI Listing

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