During the presentation, McCallum described how she is investigating the physical damage a person experiences after a spinal cord injury.
"The spinal cord is a like a freeway," explained McCallum, who works in the lab of Cedars-Sinai investigator Joshua Burda, PhD. "It allows two-way communication to connect the body and the brain. When a part of this freeway is damaged, communication is disrupted. Minimizing this damage is really key to maintaining communication."
When nerve cells die at the site of a central nervous system injury, they generate a toxic environment, which spreads into undamaged tissue and causes even more cells to die. This process is known as a secondary injury and may continue for weeks or months after the initial injury.
McCallum noticed that more cell death occurs in areas of the spinal cord where cells called astrocytes have already died. Astrocytes are essential support cells that keep the nervous system healthy. McCallum was interested in studying how astrocyte survival is controlled after an injury. To study this process, she developed and applied a gene-editing method that targets astrocytes within the injured mouse spinal cord to learn about biologic mechanisms that may aid astrocyte survival. McCallum discovered that astrocyte survival prevents cell death after spinal cord injury, restricting the size of the injury and limiting disability.
McCallum is continuing to study mechanisms that aid astrocyte survival and how these can be applied to new drugs and treatments for spinal cord injury.
Mesquita's presentation focused on his work investigating a type of heart failure that occurs when the lower left chamber of the heart cannot properly fill with blood. The condition, known as heart failure with preserved ejection fraction, currently has no effective therapies and can lead to sudden death.
"One of the explanations for why there are no effective therapies is that we don't understand the mechanisms underlying this very complex syndrome,"Mesquita said.
Scientists do know that the sinoatrial node, a group of specialized cells called located near the right atrium of the heart, helps regulate the heartbeat. By conducting exercise testing on mice, Mesquita discovered that abnormalities in electrical components of the sinoatrial node limit increases in heart rate and, consequently, exercise performance. These abnormalities could be the targets of novel therapies to treat this condition.
Mesquita conducts research under the mentorship of Eugenio Cingolani, MD, assistant professor of Medicine and director of Preclinical Research and the Cardiogenetics Program at Cedars-Sinai, and Eduardo Marbán, MD, PhD, the Mark Siegel Family Foundation Distinguished Chair and executive director of the Smidt Heart Institute at Cedars-Sinai.
Postdoctoral scientists at Cedars-Sinai will have the chance to apply for next year's award in the fall.