The study demonstrates how inflammatory activation alters mitochondrial function and anti-apoptotic gene expression in THP-1 acute myeloid leukemia cells, suggesting vital implications for disease...
The key functions of mitochondrial respiration and the expression of genes from the BCL2 and IAP families were studied in THP-1 cells from acute myeloid leukemia, both with lipopolysaccharide (LPS) and zymosan A-induced inflammation, as well as in conditions of aseptic inflammation simulating the inflammatory microenvironment. Three-dimensional cell culture was used to investigate these processes. It was found that both LPS and zymosan-A-induced inflammation and aseptic activation led to a decrease in mitochondrial membrane potential and oxygen consumption. At the same time, there was an increase in proinflammatory cytokines such as IL-1β, TNF-α, and IL-6, as well as reactive oxygen species (ROS) and lactate production. It was also found that in THP-1 cells under conditions of inflammation, there was an upregulation of the expression of genes encoding anti-apoptotic proteins, including BIRC3, BIRC7, BCL2, BCL2L1, BCL2L2 and BCL2A1.
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E.I. Meshcheriakova (2025) studied this question.
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