Researchers with LSU Health New Orleans School of Medicine believe they’ve discovered a molecular explanation for why hypoxia increases the risk for blood clots.
Lead author Rinku Majumder, PhD, and colleagues studied cultured human liver cancer cells under normal oxygen levels and hypoxic conditions. They chose those cells because Protein S (PS)—a natural anticoagulant—is mainly produced in the liver and hypoxia is common in cancer tumors, according to a press release.
At low oxygen concentrations, PS was reduced while another protein that turns on the gene to produce hypoxia was significantly increased. According to Majumder et al., this suggests the hypoxia-inducing factor 1 protein regulates PS, which they confirmed in a mouse study.
“Although discovered 40 years ago, the exact mechanism of PS's anticoagulant action was deduced only in the last few years,” Majumder said in the release. “Our earlier work found that PS inhibits a key clotting protein, Factor IXa. We knew that PS deficiency could occur in hypoxia but not why. With this study, our group identified the gene regulatory mechanism by which oxygen concentration controls PS production.”
The researchers also published their work online in the journal Blood. Majumder predicted it “will open a new direction for targeting hypoxia-mediated thrombotic disorders.”
Daniel joined TriMed’s Chicago editorial team in 2017 as a Cardiovascular Business writer. He previously worked as a writer for daily newspapers in North Dakota and Indiana.