PCMM | Highlights

February 27, 2017 

Seeking a way to keep organs young


The wear and tear of life takes a cumulative toll on our bodies. Our organs gradually stiffen through fibrosis, which is a process that deposits tough collagen in our body tissue. Fibrosis happens little by little, each time we experience illness or injury. Eventually, this causes our health to decline.

"As we age, we typically accumulate more fibrosis and our organs become dysfunctional," says Denisa Wagner, PhD, the Edwin Cohn Professor of Pediatrics in the Program in Cellular and Molecular Medicine and a member of the Division of Hematology/Oncology at Boston Children's Hospital and Harvard Medical School.

Ironically, fibrosis can stem from our own immune system's attempt to defend us during injury, stress-related illness, environmental factors and even common infections.

But a Boston Children's team of scientists thinks preventative therapies could be on the horizon. A study by Wagner and her team, published recently by the Journal of Experimental Medicine, pinpoints a gene responsible for fibrosis and identifies some possible therapeutic solutions.

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June 23, 2016 

Denisa Wagner Received William Harvey Medal from William Harvey Institute. London, UK

Dr. Denisa Wagner was honored with the William Harvey Medal during the 30th Anniversary Conference of the William Harvey Research Institute. Dr. Wagner also gave the Derek Willoughby Lecture.

June 22, 2015

Denisa Wagner Received the 2015 Grant Medal, the highest award of the International Society on Thrombosis and Haemostasis (ISTH)

Wagner, a former member of the ISTH Council (2004-10), is the Edwin Cohn Professor of Pediatrics at Harvard Medical School in Boston. She grew up in Prague and received her Diploma of Biochemistry from the University of Geneva in Switzerland and her Ph.D. in biology from the Massachusetts Institute of Technology.

Among her many accomplishments, Wagner is credited with defining the cell biology of von Willebrand factor and uncovering the biological importance of P-selectin as well as the importance of neutrophil extracellular traps (NETs) in thrombosis and sterile inflammation. Wagner and her colleagues were the first laboratory to study thrombosis, using the now widespread technique of intravital microscopy, in genetically-engineered mice.

Wagner currently serves as a member of the Program in Cellular and Molecular Medicine and the division of hematology/oncology at Boston Children’s Hospital. For many years, the Wagner Laboratory’s research has focused on adhesion molecules and their function in normal physiology and in pathological situations. They have engineered mice lacking platelet, endothelial or leukocyte adhesion receptors. The Wagner Lab is particularly interested in the interplay of inflammation and thrombosis. Current research efforts explore the role of neutrophils and the impact of NETs in physiological and pathological processes such as cancer-associated thrombosis, deep vein thrombosis and wound healing.

Wagner has received numerous other awards for her work as a recognized leader in the field of thrombosis and hemostasis. The ISTH previously awarded her with the Distinguished Career BACH Award in 2005.The Robert P. Grant Medal is the highest award of the ISTH. It is presented at each biennial Congress of the Society to a recipient selected for outstanding service or accomplishment who has promoted the goals of the Society. This award may be for research achievement, for organizational activities, for important public recognition and support of research activities, for facilitation of institutional cooperation and communications, for unusual teaching or educational initiatives, or for the development of concepts which result in a clearer understand of the meaning of research data.

Robert P. Grant (1915-1966) was a renowned cardiologist with interdisciplinary interests. He served on the staff and ultimately became director of the National Heart Institute in Bethesda, Md., USA, and also served as a representative of the National Institutes of Health in Europe.

June 15, 2015

How our neutrophils might sabotage wound healing in diabetes

By Tom Ulrich

When you get a cut or a scrape, your body jumps into action, mobilizing a complicated array of cells and factors to stem bleeding, keep the wound bacteria-free and launch the healing process.

For most of us, that process is complete in a couple of weeks. But for many people with type 1 and type 2 diabetes, delayed wound healing can have permanent consequences. For example, between 15 and 25 percent of diabetes patients develop chronic foot ulcers. Those ulcers are the root cause of roughly two-thirds of lower limb amputations related to diabetes.

Why don’t these wounds close? Blame a perfect storm of diabetic complications, such as reduced blood flow, neuropathy and impaired signaling between cells. According to research by Denisa Wagner, PhD, of Boston Children’s Hospital’s Program in Cellular and Molecular Medicine, a poorly understood feature of our immune system’s neutrophils may be one more ingredient in the storm.

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