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• W2054981443 abstract "In Brief Objective: We investigated whether Kupffer cell phagocytosis is differentially regulated following hypoxia (by breathing hypoxic gas) and trauma-hemorrhage. We hypothesized that the differences might result from a differential activation of hypoxia-inducible factor (HIF)-1α and phosphoinositide 3-kinase (PI3K)/Akt pathway under those conditions. Background: HIF-1α is a biologic O2 sensor enabling adaptation to hypoxia. Studies have shown that under hypoxic conditions, HIF-1α enhances macrophage phagocytosis. Trauma-hemorrhage also produces a hypoxic insult with HIF-1α activation; however, macrophage phagocytosis is suppressed under those conditions. Thus, signaling molecules other than HIF-1α should be taken into consideration in the regulation of macrophage phagocytosis following cellular hypoxia or trauma-hemorrhage. Methods: Male C3H/HeN mice were subjected to sham operation, trauma-hemorrhage (laparotomy, 90 minutes hemorrhagic shock, MAP 35 ± 5 mm Hg followed by resuscitation) or hypoxia (5% O2 for 120 minutes). The trauma-hemorrhage and hypoxia groups received Wortmannin (PI3K inhibitor), YC-1 (HIF-1α inhibitor) or vehicle at the time of maximum bleedout in the trauma-hemorrhage group or at a PaO2 of 30 mm Hg during hypoxic air inhalation. Mice were killed 2 hours later and samples/cells collected. Results: While the systemic and Kupffer cell hypoxic states were similar in the trauma-hemorrhage and hypoxia groups, phagocytic capacity was suppressed following trauma-hemorrhage but enhanced in the hypoxia group. Kupffer cells from both groups showed increased HIF-1α activation, which was prevented by Wortmannin or YC-1 treatment. The increase in Kupffer cell phagocytosis following hypoxemia was also prevented by Wortmannin or YC-1 treatment. Akt activation was suppressed in the trauma-hemorrhage group, but enhanced in the hypoxia group. Wortmannin and YC-1 treatment prevented the increase in Akt activation. Conclusions: These findings indicate that the suppression of Kupffer cell phagocytosis following trauma-hemorrhage is independent of cellular hypoxia and activation of HIF-1α, but it is possibly related to suppression of the Akt activation. Hypoxia-inducible factor-1α is up-regulated under hypoxic conditions as well as following trauma-hemorrhage and plays an important role in regulating immune cell activities. Kupffer cell phagocytosis was enhanced following hypoxia but was suppressed following trauma-hemorrhage, thus revealing the crucial role of phosphoinositide 3-kinase/Akt activation in hypoxia-inducible factor-1α-mediated regulation of phagocytosis." @default.
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• W2054981443 date "2009-12-01" @default.
• W2054981443 modified "2023-10-17" @default.
• W2054981443 title "Trauma-Hemorrhage and Hypoxia Differentially Influence Kupffer Cell Phagocytic Capacity" @default.
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• W2054981443 doi "https://doi.org/10.1097/sla.0b013e3181b0ebf8" @default.
• W2054981443 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2814123" @default.
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