Individuals caught sitting in tight airplane seats for a whole long-haul flight are vulnerable to harmful blood clots. However by some means motionless, hibernating bears will not be. Now scientists know why.
Bears settled in for winterlong slumbers have low ranges of a key protein that helps blood clots type, researchers report within the April 14 Science. Platelets missing this protein don’t simply stick collectively, defending the animals from creating probably harmful blood clots. And low ranges of the protein will not be simply discovered bears, the staff writes. Mice, pigs and people with a largely sedentary life-style due to long-term mobility issues have the identical safety.
The research is a “large step ahead,” says Tinen Iles, a computational biologist on the College of Minnesota in Minneapolis who was not concerned with the analysis. It introduced collectively researchers from all kinds of backgrounds — from wildlife biologists to well being care consultants — to point out how animals have tailored to cease immobility-related blood clots. Now, researchers have a roadmap to imitate nature’s options with medicine.
Warmth shock protein 47, or HSP47, is generally discovered within the cells that make up connective tissues like bone and cartilage. It’s additionally present in platelets, the place HSP47 attaches to collagen, a protein that helps platelets stick collectively. That is useful when the physique responds to a minimize or different damage; it’s harmful when a clump of platelets blocks blood circulation to the lungs. Potential medicine primarily based on this research’s discovering would goal to cease HSP47 from interacting with proteins or immune cells that spark clots, says Tobias Petzold, a heart specialist at College Hospital at Ludwig-Maximilians-Universität München.
Staying nonetheless for lengthy intervals of time — like throughout air journey — can put individuals vulnerable to creating deep vein thrombosis, uncommon however harmful blood clots that normally take form within the legs (SN: 6/13/06). Throughout such intervals of inactivity, irritation and gradual blood circulation could make clots extra more likely to type.
Hibernating bears spend months in a dormant state, decreasing their coronary heart charge under what’s typical in lively months. However research have advised that the animals don’t die of circumstances linked to blood clots in veins throughout hibernation (SN: 2/10/12). What’s extra, individuals who expertise long-term immobility, similar to these with spinal twine accidents, don’t develop extra clots than individuals with typical mobility, Petzold says. However it was unclear why motionless bears and a few persons are shielded from probably lethal clots.
Petzold and colleagues analyzed blood samples from 13 wild brown bears (Ursus arctos) in winter and summer time. Platelets from blood samples taken throughout hibernation had been much less more likely to clump collectively than summer time samples, and ones that did clot did so extra slowly. That seasonal distinction was pinned to HSP47 in platelets: In hibernating bears, ranges of the protein had been about one-fiftieth the quantity present in lively animals.
To verify that HSP47 might be behind the bears’ lack of blood clots, the staff did lab checks with mice. Mice missing the protein had fewer clots and decrease ranges of irritation than animals that did have HSP47. What’s extra, pigs that had lately given start — rendering them largely motionless for as much as 28 days whereas feeding their piglets — additionally had decrease HSP47 ranges in contrast with lively pigs.
These findings prolong to individuals, too. Individuals with long-term immobility due to spinal twine damage had low ranges of HSP47 and no different indicators of inflammation-related clotting. The identical was additionally true amongst 12 in any other case wholesome individuals who spent a month taking part in a voluntary mattress relaxation research. After 27 days of immobility, their HSP47 ranges went down.
Total, most animals use comparable proteins and cells to make clots and forestall blood loss, says Marjory Brooks, a veterinarian and comparative hematologist at Cornell College who wasn’t concerned within the research. However there could also be some variation amongst species within the sequence of occasions that come earlier than the clot.
Understanding how human our bodies particularly regulate HSP47 is necessary in order that potential medicine discover the precise stability between stopping clots and an excessive amount of bleeding.
The following massive query to deal with, Petzold says, is how motionlessness prompts the physique to make much less HSP47.
