Karin Hoffmeister

In a study published in Nature Medicine, Karin Hoffmeister, MD, associate biologist at Brigham and Women’s Hospital, describe a new feedback mechanism that helps control the production and removal of platelets – cells that help stem bleeding – from circulation in the bloodstream. The new findings may help illuminate how certain platelet diseases develop and could point researchers to potential targets for future drug development.

The researchers report that old (senescent) platelets are recognized and removed from circulation by a receptor known as the Ashwell-Morell receptor (AMR) on liver cells. The researchers found that over time, platelets lose a particular sugar known as sialic acid. The AMR removes these older platelets from circulation and signals, through JAK2 and STAT3 receptors, for new platelets to be produced. The current study finds that the AMR’s removal of older platelets is a critical control point for thrombopoietin – a known regulator of platelet production.

The AMR was discovered four decades ago, but its role has been elusive until now.

“The connection between the liver and the bone marrow never ends – the platelets inform the liver about the status of the bone marrow, making a loop,” said Hoffmeister, who is also an associate professor of Medicine at Harvard Medical School. “This mechanism, where we show how the platelets talk to the liver, helps complete that circle.”

The work could have potential implications for blood transfusions. Currently, platelets must be collected over multiple sessions from a donor in order to harvest enough for a transfusion. Platelets have only a five-day shelf life after collection, further complicating the donation and collection process.

“If we could find ways to encourage platelet production before transfusion, we could use the system to have more platelets per collection from the donor,” said Hoffmeister.