Bio: Dr. Qian Ran is a Full Professor at the Army Medical University, where she also obtained her Ph.D. in Clinical Laboratory Diagnostics. She was ever worked as a visiting scholar in University of Southern California in Los Angeles, US (2015-2016). Her main research areas include uncovering the mechanisms of bone marrow hematopoietic radiation injury and exploring innovative therapy strategies. She has identified several key regulatory molecules of radiation-induced hematopoietic injury as potential therapeutic targets, and pre-clinical studies are currently underway to develop small molecule inhibitors and modify cytokine based on these discoveries. Related research was published on JACS, PNAS, Mil Med Res and Biomaterials et al. Dr. Qian Ran has received prestigious honors such as the First Prize for Chongqing Scientific and Technological Progress and Second Prize for Military Medical Achievements.  

Abstract: Poor hematopoietic recovery is the main cause of death in radiation exposure, and hematopoietic repair is the key to the treatment of acute radiation syndrome in bone marrow. Our study found that the radiation tolerance of endothelial cells (EC) was much higher than that of hematopoietic stem cells (HSC), and they may play an important role in hematopoietic repair. Through single-cell sequencing experiments, we identified a unique subpopulation of hematopoietic endothelial cells (cKit+Cd34+Cd38+Sca-1+Cd150+Cdh5+Cd31+Cd200+) co-expressing hematopoietic and endothelial markers in the sinusoidal niche, and confirmed Cdh5+Cd200+ dual expression as the definitive signature of this subpopulation. This subpopulation may be generated by sinusoidal EC through endothelial hematopoietic transformation (EHT), and its expression profile is more similar to that of long-term HSC. The number of this subpopulation was positively correlated with the number of HSC, the degree of proliferation of bone marrow cells, and the recovery of peripheral blood count after radiation. In vitro, we found that this subpopulation had the ability to differentiate into erythroid, granulocytic, and monocyte lineage blood cells. In summary, we found that radiation can trigger a process similar to EHT in embryonic development, which is of great significance in promoting the repair of bone marrow hematopoietic damage.