Although they remain lying and almost motionless for several months, brown bears do not develop thrombosis during hibernation. This is made possible by a special mechanism that researchers have now identified and have been able to demonstrate, among other things, in people with spinal cord injury.
Immobility is one of the greatest risk factors for potentially life-threatening venous thromboembolism. For example, people who have been bedridden for weeks have an increased risk of thrombosis. In the case of paraplegics, this danger is averted after the acute phase of the injury – just like in the case of brown bears in hibernation.
An international research team led by Dr. Tobias Petzold from the Ludwig Maximilian University Hospital in Munich and Prof. Matthias Mann, Director of the Max Planck Institute for Biochemistry in Martinsried, got to the bottom of it. The results of their recently published Study provide a starting point for the development of preventive therapies for immobilized acute patients.
Searching for clues in blood samples from brown bears
As part of their collaboration with Prof. Ole Fröbert from the University Hospital in Örebro, Sweden, the researchers traveled to central Sweden once in summer and once in winter. A population of brown bears has been studied there for more than ten years. The study authors used GPS transmitters to locate the animals, sedated them and took blood from them. They then released the bears back into the wild.
The fresh samples were analyzed in a mobile laboratory within three to four hours. At first glance, there were no relevant differences between samples taken in summer and winter. However, more detailed analysis later showed that in hibernating brown bears, the interaction between blood platelets and inflammatory cells of the immune system is inhibited.
Protein regulates interaction with platelets
In order to uncover the molecular mechanisms behind this, the team went in search of altered proteins in the brown bears’ blood. To do this, the scientists carried out mass spectroscopy-based proteomics. They identified 71 platelet proteins that are upregulated in bears during hibernation and 80 platelet proteins that are downregulated.
The biggest difference between hibernating and active bears was the heat shock protein 47 (HSP47), which can activate inflammatory cells. HSP47 was downregulated 55-fold in hibernating bears. This also explains the reduced interaction between blood platelets and inflammatory cells, which protects the animals from thrombosis.
Evolutionarily conserved thrombosis protection
HSP47 downregulation with prolonged immobilization also occurs in other mammals such as mice and humans. The researchers were able to observe them, among other things, in paraplegic subjects who took part in a study by the German and American space agencies and were on bed rest for three weeks.