Microfluidic and Spleen-on-a-Chip Studies of Sickle Cell Disease

Presented By: Ming Dao, PhD
Speaker Biography: Ming Dao is the Director and Principal Investigator of MIT’s Nanomechanics Laboratory. He is a Fellow of the American Society of Mechanical Engineers (ASME) and named the 2012 Singapore Research Chair in Bioengineering and Infectious Disease by MIT. He had been a visiting/adjunct professor with the National Institute of Blood Transfusion, France (2016-2017), Xi’an Jiaotong University, China (2011-2020) and Nanyang Technological University, Singapore (2018-present). His broad research interests include cell biomechanics/biophysics of human diseases, nanomechanics of advanced materials, and machine learning for engineering and biomedical applications. He has published more than 160 papers in peer-reviewed journals, including Science, Nature Materials, Science Advances, Nature Communications, Proceedings of the National Academy of Sciences, etc. He is ranked as a Top 2% Scientist by Ioannidis/Stanford University and a top 0.5% researcher in both citation and h-index by Exaly.com. He has also chaired or co-chaired 18 international symposiums/workshops/webinar series.
Webinar: Microfluidic and Spleen-on-a-Chip Studies of Sickle Cell Disease
Webinar Abstract: Healthy human red blood cells (RBCs) gradually degrade over their lifespan of ~120 days. However, sickle cells - RBCs from sickle cell disease (SCD) patients - degrade much faster within their much-shortened lifespan of ~10-20 days. Understanding the underlying mechanisms of RBC senescence in health and disease is crucial for studying many RBC diseases. Both normal RBCs and sickle cells experience repeated cycles of hypoxia and mechanical fatigue. To investigate the impact of these challenges on RBC damage and degradation accumulation, we developed in vitro microfluidic assays for testing RBCs under cyclic hypoxia loading and/or cyclic mechanical loading. Moreover, spleen plays a crucial role in maintaining the balance between RBC formation (erythropoiesis) and removal. Altered RBCs are cleared from circulation through splenic RBC retention and elimination, which mainly occur in open circulation, where RBCs flow through macrophages and inter-endothelial slits (IESs). Specifically, we developed an in-vitro oxygen-mediated spleen-on-a-chip platform, combined with in-silico simulations and in-vivo/ex-vivo observations to study spleen function and antisickling drug efficacy. Our results provide mechanistic insights into how spleen maintains its homeostatic balance between splenic RBC retention and elimination, and how disruptions in this balance could lead to anemia, splenomegaly, and acute splenic sequestration crisis in SCD.
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