| Seminar: Myelin-laden Macrophage: The True Villain Behind Spinal Cord Injury Speaker: Yi Ren, Professor of Medicine and Immunology, Florida State University College of Medicine, Florida, USA. Time: 3pm, Friday afternoon, October28， 2016 Place: 中科大中区医学楼5层会议室
报告人简介： Dr. Yi Ren received PhD in Cell Biology from Imperial College London, UK. Dr. Ren Laboratory’s primary focus is to determine what factors influence macrophage inflammatory activation and their function during the resolution of spinal cord injuries. Dr. Ren was the first to discover that transfer of the scavenger receptor CD36 gene into non-phagocytic cells conferred the ability to clear of apoptotic cells (J. Exp. Med), the finding has been cited more than 500 times. The long-term significance of this work has become increasingly apparent, as we learn that clearance of dying cells is important to not only promoting resolution of injury- and infection-related inflammatory responses but also the pathology of other diseases, including cancer. In addition, Dr. Ren has also published extensive works on macrophage function in prestigious journals including Journal of Clinical Investigation, the Journal of Immunology, Am J. Pathology, and Cell Death and Differentiation, PNAS, Cancer Research, Oncogene, and Clinical Cancer Research, etc. These papers have been extensively cited, recognized and awarded a highly prestigious The UK Royal Society. Dr. Ren’s outstanding research works have been funded by US NSF, NIH, and various foundations.
Abstract of the seminar: Spinal cord injury (SCI) provokes an inflammatory response that causes secondary tissue damage and neurodegeneration. Much of the secondary tissue damage stems from inflammation ocrchestrated by the accumulation of bone marrow derived macrophages (Mf) within the epicenter of the injured spinal cord. Among other things, the infiltrated Mf engulf myelin debris to form myelin-laden macrophages (mye-Mf). The mye-Mf persist in the injured spinal cord for long periods of time, which promotes disease progression due to their pro-inflammatory phenotype, enhanced neurotoxicity and impaired phagocytic capacity for apoptotic cells. Recently, we discovered that mye-Mf (but not normal Mf) injected into a normal spinal cord become immobilized at the site of injection and cause pathogenic changes in the spinal cord, including inflammatory cell infiltration and axon demyelination. Our in vitro experiments further demonstrated that exosomes released by mye-Mf stimulate inflammatory responses and inhibit neuronal differentiationof neural stem cells. We therefore propose that the excessive accumulation of mye-Mf contributes to secondary injury through two parallel mechanisms: 1) mye-Mf secrete exosomes that directly contribute to inflammatory responses, and 2) mye-Mf have an impaired phagocytic capacity for apoptotic cells, including infiltrated neutrophils, at the injured site. This impaired phagocytic capacity allows infiltrated neutrophils to undergo secondary necrosis and to release their toxic contents, resulting in secondary injury. Our central hypotheses are the excessive accumulation of mye-Mf is the root of secondary injury and targeting mye-Mf could represent an efficient strategy to improve local inflammatory microenvironment in injured spinal cord and motor neuron function recovery. We expect to demonstrate the pathophysiological roles of mye-Mf in SCI, and provide experimental support for novel therapeutic interventions. 报告联系人：申勇教授实验室 |
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