Stories about: deep vein thrombosis

“Shapeshifter” that regulates blood clotting is visually captured for the first time

GIF of VWF, which regulates blood clotting, elongating and relaxing on loop
A single molecule of von Willebrand factor is visually captured, as it elongates and relaxes in response to blood flow conditions, for the very first time. Credit: Springer/Wong labs (Boston Children’s Hospital and Harvard Medical School)

We are normally born with a highly sophisticated array of molecules that act as “sentries,” constantly scanning our bodies for injuries such as cuts and bruises. One such molecular sentry, known as von Willebrand factor (VWF), plays a critical role in our body’s ability to stop bleeding.

To prevent hemorrhage or life-threatening blood clots, VWF must strike a delicate balance between clotting too little or too much. Researchers have long suspected that the mechanical forces and shear stress of blood flow could be closely-related to VWF’s function.

“In some ways, like in the movie Star Wars, VWF may be considered a Jedi knight in our body that can use ‘the force’ to guard the bloodstream,” says Timothy Springer, PhD, of Boston Children’s Hospital and Harvard Medical School (HMS).

It has not been possible to witness exactly how VWF senses and harnesses these mechanical forces — until now.

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Catching platelets with NETs: Neutrophils and deep vein thrombosis

Sea cucumbers drive off attackers by expelling their innards. Neutrophils do the same, forming NETs to fight bacteria. But that same capability might also help fuel dangerous blood clots. (Anders Poulsen/Wikimedia Commons)

Sea cucumbers have an unusual way of defending themselves. When threatened, they ensnare their foes with sticky threads. Some even expel their own internal organs to repel attackers.

Immune system cells called neutrophils sometimes do much the same: When confronted with bacteria, they unravel and shoot out their chromatin—the tightly wound mix of DNA and proteins that keeps genes packaged in cells. The resulting molecular mesh, known as a neutrophil extracellular trap, or NET, traps and kills bacteria, providing an additional line of defense against bloodstream infections.

But neutrophils and NETs can go awry. Since 2010, Denisa Wagner, PhD, of the Program in Cellular and Molecular Medicine at Boston Children’s Hospital, has been studying NETs’ role in deep vein thromboses (DVTs)—blood clots that form in veins deep in the body where blood clots shouldn’t, usually in the legs.

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“Good” cholesterol could be even better for you than you thought

When you get on a long flight, there's always a risk of developing a deep vein thrombosis (DVT): a blood clot in your legs. But "good" cholesterol may be able to help stop DVTs from happening. (randomduck/Flickr)

Most of us are familiar with “good” and “bad” cholesterol. Low-density lipoprotein (LDL) is “bad” because it keeps cholesterol in the body, while the “goodness” of high-density lipoprotein (HDL) stems from its ability to scoop up old, used cholesterol and escort it to the liver for disposal. Because high levels of HDL in the blood are associated with lower risk of cardiovascular disease (a link that has recently come under question), it has received much attention from researchers.

And anyone who travels a great deal has probably heard about deep vein thrombosis or DVT, often cited as a good reason to get up and stretch your legs on a long flight. Restriction of normal blood flow—whether from being bedridden, paralyzed or sitting for hours on airplanes—is a major cause of blood clots in the legs. Though these clots can be painful in and of themselves, if they break free and travel to the lungs they can cause a potentially fatal pulmonary embolism. In fact, DVTs afflict nearly a million Americans each year and claim a quarter of a million lives.

Now a team from the lab of Denisa Wagner, PhD, of Boston Children’s Hospital’s Program in Cellular and Molecular Medicine and the Immune Disease Institute (PCMM/IDI), directed by Alexander Brill, MD, PhD, has found a connection between “good” cholesterol and DVT that may change the way these dangerous clots are treated—and perhaps prevented.

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