Regardless of spending greater than half the 12 months hibernating in frigid temperatures, brown bears (Ursus arctos) stay remarkably wholesome. These idle giants not often endure from maladies reminiscent of blood clots, which might happen in people experiencing solely momentary bouts of immobility and might be lethal. “Sufferers who come into the hospital with a damaged leg are often susceptible to develop thrombosis,” says Tobias Petzold, a heart specialist on the German Heart for Cardiovascular Analysis. “However in distinction, brown bears, that are mendacity round for a few months, don’t develop clots.”
In a brand new research printed on Thursday within the journal Science, Petzold and his colleagues pinpointed a protein that helps the hibernating bears avoid dangerous clotting that may forestall blood circulation throughout their lengthy winter slumber.
To find out how dormant bears maintain blood pumping throughout months of torpor, Petzold and his colleagues partnered with biologists finding out a inhabitants of brown bears in Sweden. The biologists collected blood samples from 13 hibernating bears of their dens in the course of the winter. In the summertime the biologists collected extra blood from the identical bears after taking pictures tranquilizer darts at them from a helicopter.
The researchers then ran these samples by means of a battery of blood exams. They found that the portions of greater than 150 proteins various vastly between the blood of hibernating and energetic bears and homed in on the proteins in platelets—the elements of blood that trigger clotting. The platelet protein with the biggest disparity between energetic and hibernating bears was warmth shock protein 47 (HSP47).
HSP47 recruits an enzyme known as thrombin that helps platelets stick collectively and kind clots. In energetic bears, HSP47 helps patch up cuts and cease bleeding. However hibernating bears, that are safely comfortable of their dens, have little use for this clotting protein. On common, hibernating bears’ platelets produced 55 occasions fewer HSP47 proteins than these of energetic bears.
“We hadn’t heard a lot about this protein, and we have been fully shocked to find that it has such a big affect,” says Manuela Thienel, the paper’s lead creator, additionally on the German Heart for Cardiovascular Analysis. Thienel says that reducing the degrees of this explicit protein doubtless reduces the platelets’ penchant for clumping collectively and proscribing blood circulation.
Mirta Schattner, a biologist on the Laboratory of Experimental Thrombosis and Immunobiology of Irritation on the Institute of Experimental Medication in Argentina, agrees. “This mobile interplay [of HSP47 proteins] is useful when restricted and is [also] crucial for holding infections” and irritation, says Schattner, who was not concerned with the analysis workforce however wrote a commentary on the new study in Science.
To find out if an identical mechanism prevents blood clotting in chronically motionless people, the researchers in contrast blood samples from sufferers who had suffered debilitating spinal accidents with samples from their energetic counterparts. Like that of hibernating bears, the blood of chronically motionless sufferers had fewer circulating HSP47 proteins. “Downregulation of HSP47 throughout hibernation of bears or chronically immobilized sufferers reduces thromboinflammation” and thus reduces the chance of blood clots, Schattner says.
The workforce additionally collected blood from a number of wholesome people earlier than they participated in a month-long spaceflight simulation research run by NASA and the German Aerospace Heart. After the individuals’ skilled 27 days of head-down mattress relaxation, the researchers collected one other spherical of samples to see how the extended immobilization had impacted their physiology. The workforce found that the individuals’ platelets started to supply considerably much less HSP47 over the course of their experimental immobilization.
The researchers discovered an identical sample within the blood of mobility-limited pigs and lab-bred mice. They posit that lowering the expression of HSP47 proteins could also be a mechanism used throughout mammals to forestall clotting throughout extended durations of relaxation. However this strategy seems to take time to develop—in people, individuals experiencing shorter-term immobility from sickness or harm are extra vulnerable to clotting than chronically motionless individuals with spinal twine accidents.
Petzold says the brand new findings spotlight how understanding the biology of bears and different animals can present insights into how the human physique capabilities. And so they might probably encourage fine-tuned remedies for stopping clotting in sufferers experiencing momentary immobility. “By taking a look at how hibernating bears in nature forestall clots, we now know that people do the identical factor to forestall blood clots,” he says.
