Red Blood Cell Function, Creation and Renewal the Focus of Sickle Cell Conference Symposium

Scientists discuss self-renewal, sickling prevention and novel treatment approaches

Article ID: 684585

Released: 3-Nov-2017 3:25 PM EDT

Source Newsroom: American Physiological Society (APS)

Newswise — Washington (November 8, 2017)—Researchers will meet to discuss the physiology, function and future of red blood cells (RBCs) in sickle cell disease (SCD) at the “Red Cell Physiology” symposium during the American Physiological Society’s Physiological and Pathophysiological Consequences of Sickle Cell Disease conference in Washington, D.C.

RBCs are center stage in SCD, a chronic genetic condition in which the cells form in an abnormally sickled shape. Sickled RBCs cause interruption of blood flow and episodes of significant pain in people with SCD. The Red Cell Physiology symposium “will include several presentations that will discuss physiology of RBCs and mechanisms of their renewal,” said symposium chair Sergei Nekhai, PhD, of Howard University in D.C. Speakers will include James Palis, MD, from the University of Rochester Medical Center in New York and Mohandas Narla, DSc, of the New York Blood Center.

People with SCD often need blood transfusions to minimize symptoms. Shortages in local and national blood supplies and adverse reactions to donor blood can complicate treatment. New ways to create RBCs, either inside or outside the human body, may help alleviate these challenges. Palis will discuss the renewal of RBC in his presentation, “Developmental Regulation of Erythroid Self-Renewal.” Palis’ lab has identified a protein that may become an important factor in self-renewal.

Narla will discuss new treatment options that are focused on preventing RBCs from sickling and from sticking to the lining of the blood vessels (endothelium) in his talk, “Pathobiology of Sickle Red Cells: Implications for Pathophysiology of Sickle Cell Disease.” Two approaches include stopping dehydration in RBCs—a trigger for sickling—and reactivating fetal hemoglobin in the body. Fetal hemoglobin, an oxygen-carrying protein present in the body before birth, does not contain the mutation that causes SCD. Most people stop producing fetal hemoglobin in infancy, at which point the mutated form of adult hemoglobin appears in people affected by SCD. Turning fetal hemoglobin back on may prevent the formation of the mutated RBCs, which can ease symptoms of the disease.

The Red Cell Physiology symposium will be held on Wednesday, November 8, from 1:30 to 3:30 p.m. in the Embassy Suites D.C Convention Center Hotel.

NOTE TO JOURNALISTS: The Physiological and Pathophysiological Consequences of Sickle Cell Disease conference will be held in Washington, D.C., November 6–8, 2017. Read the full program. To schedule an interview with the conference organizers or presenters, contact the APS Communications Office or call 301-634-7209. Find more research highlights in the APS Press Room.

Physiology is the study of how molecules, cells, tissues and organs function in health and disease. Established in 1887, the American Physiological Society (APS) was the first U.S. society in the biomedical sciences field. The Society represents more than 10,500 members and publishes 15 peer-reviewed journals with a worldwide readership.

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