Hibernating Bears Give People Ideas to Prevent Clots

Winter Sleeping Bears Give People Ideas on Preventing Clots
Winter Sleeping Bears Give People Ideas on Preventing Clots

Sleeping giants are protected from blood clots thanks to low levels of the clotting factor HSP47, and mammals like humans and other humans may be similarly protected.

Long flights increase the risk of blood clotting disorders such as deep vein thrombosis because prolonged inactivity causes the veins to bend, allowing blood to pool and possibly clot. However, hibernating animals such as bears and ground squirrels do not have this problem.

The reason why hibernating bears rarely experience blood clots is now better understood, according to a study published April 13 in the journal Science. The scientists discovered that when bears hibernate, they reduce the production of the heat shock protein 47 (HSP47), which is usually found on the surface of platelets and helps them bind to collagen. The study revealed that humans and pigs also reduced HSP47 production during periods of inactivity, showing that this phenomenon is not unique to bears. The research could help identify individuals who are vulnerable to venous thromboembolism, also known as deep vein thrombosis and pulmonary embolism, and pave the way for potential future treatments.

One of the main causes of death worldwide is blood clots. Scientists have long been puzzled by this clinical problem, according to Thomas Renné, a chemist at the Hamburg-Eppendorf University Medical Center who was not involved in the study but has previously worked with some of the authors.

The researchers selected this rare model species for their study to understand why Swedish grizzly bears (Ursus arctos) rarely develop blood clots while hibernating. The Scandinavian Brown Bear Research Project, which has been working on brown bear ecology in Sweden and Norway for the past 30 years, also collaborated on the study.

Researchers roamed the snow-capped mountains and forests of northern Sweden in February and March of 2019 and 2022, looking for hibernating bears. The giant bears were anesthetized and blood samples were taken when researchers found the GPS-tagged creatures. This process was repeated the following June, and a helicopter was used to locate the bears, which had been much more vicious by then. Between the two events, a total of 13 bears' blood was found.

Tobias Petzold, an immunologist at Ludwig-Maximilians University in Munich and co-author of the study, remembers that the researchers set up a temporary laboratory close to the site because samples needed to be examined immediately. “We brought the blood to this romantic, red-painted wooden house with its scientific instruments,” he explains. The researchers drew on a series of in vitro platelet physiology studies to determine how hibernating grizzly bears can be protected from clot formation.

Biological components such as platelets, immune cells, and collagen all contribute to clot production. However, collagen-induced activation of platelets is a very important step. After the platelets adhere to the collagen in the blood vessel wall, they clump together. However, the presence of collagen inhibited the aggregation of platelets of hibernating bears. In addition, a mass spectrometry study showed that platelets produce approximately 55 times less HSP47 in hibernating bears than in their summer counterparts. Along with other collagen receptors involved in thrombosis, this protein also participates in collagen signaling on platelets. According to Petzold, “protein is highly conserved in the animal kingdom.” Researchers also discovered thromboinflammation.

Therefore, the researchers developed knockout mice lacking HSP47 to examine whether the protein actually confers an anticoagulant function in other species. They discovered that the mice formed smaller clots when their blood flow was reduced. Pigs that were lactating and immobilized for periods of 21 to 28 days also had lower platelet HSP47 levels compared to pigs that were not lactating. The researchers discovered similar patterns in human spinal cord injury patients because these patients had lower platelet HSP47 levels than healthy, age-appropriate controls. Petzold says it's "really surprising to us" that it's such a conserved process.

It's intriguing that they can replicate this in other species, says Scott Cooper, a biologist at the University of Wisconsin at La Crosse, who wasn't involved in the study but praising the "very comprehensive" nature of the research.

It also makes sense from an evolutionary standpoint, he continues.

The findings have obvious clinical implications, according to Renné. “We do a lot of testing on patients at high risk of developing venous and arterial thrombosis. "Many factors are known to contribute to thrombosis," he says. Based on the results of this study, you can “easily do an assay to measure the levels of this heat shock protein” and determine if it is a risk factor. He continues by suggesting that the protein may one day serve as a therapeutic target for venous thromboembolism.

Source: the-scientist.com/news-opinion

Günceleme: 16/04/2023 01:09

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