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Archive - Sep 4, 2019

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Immune Cells (Neutrophils) Drive Gallstone Formation; Finding May Open Door to New Therapeutic Interventions

Sticky meshworks of DNA and proteins extruded by white blood cells called neutrophils act as the glue that binds together calcium and cholesterol crystals during gallstone formation, researchers in Germany report in an article published online on August 15, 2019 in Immunity. The article is titled “"Neutrophil Extracellular Traps Initiate Gallstone Formation.” Both genetic and pharmacological approaches that inhibited the formation of these so-called neutrophil extracellular traps (NETs) reduced the formation and growth of gallstones in mice. "Neutrophils have long been considered the first line of defense against infection and have been shown to generate NETs that entangle and kill pathogens," says senior study author Martin Herrmann, MD, PhD, an immunologist at Universitätsklinikum Erlangen in Germany. "Here, we provide additional evidence for the double-edged-sword nature of these NETs by showing that they play an important role in the assembly and growth of gallstones. Targeting neutrophils and NET formation may become an attractive instrument to prevent gallstones in high-risk populations." Gallstones (image) are hard, pebble-like pieces of material that may be as small as a grain of sand or as large as a golf ball. They form in a pear-shaped organ called the gallbladder, which releases bile to the small intestine through the bile ducts during meals to help break down fat. Although most people with gallstones do not have symptoms, they can cause abdominal pain, nausea, and vomiting, and they are a leading cause of hospital admissions worldwide. Surgery to remove the gallbladder is one of the most common operations performed on adults in the United States.

Normal Cells Show Transient Induction of Telomerae Just Before Cell Death, Mediating Senescence and Reducing Tumorigenesis

New research from the University of Maryland (UMD) and the National Institutes of Health reveals a new role for the enzyme telomerase. Telomerase's only known role in normal tissue was to protect certain cells that divide regularly, such as embryonic cells, sperm cells, adult stem cells, and immune cells. Scientists thought telomerase was turned off in all other cells, except in cancerous tumors where it promotes unlimited cell division. The new study found that telomerase reactivates in normal adult cells at a critical point in the aging process. Just before cell death, a burst of telomerase buffers cells from the stresses of aging, slowing the process and reducing DNA damage that could lead to cancer. The study was published in the Proceedings of the National Academy of Sciences on September 2, 2019. The open-access article is titled” Transient Induction of Telomerase Expression Mediates Senescence and Reduces Tumorigenesis in Primary Fibroblasts.” "This study reshapes the current understanding of telomerase's function in normal cells,"said Kan Cao, PhD, senior author of the study and an Associate Professor of Cell Biology and Molecular Genetics at UMD. "Our work shows, for the first time, that there is a role for telomerase in adult cells beyond promoting tumor formation. We can now say that regulated activation of telomerase at a critical point in a cell's life cycle serves an important function." Telomerase prevents the shortening of telomeres--a specialized DNA-protein structure at the end of a cell's chromosomes that protect the chromosomes from damage (shown lighted up in image). Telomerase plays a critical role during embryonic development and stem cell differentiation, when cells divide profusely.