Single cell RNA sequencing of post-radiation mouse jejunum with or without DIZE

In a radiation mass casualty event, exposed populations will suffer dose-dependent toxicity to multiple-organ systems. Although several therapies are FDA-approved for treatment of the hematopoietic acute radiation syndrome (H-ARS), there are no FDA-approved medical countermeasures (MCM) for either acute gastrointestinal injury (GI) or late multi-organ toxicities known as the delayed effects of acute radiation exposure (DEARE). Prior data suggest activation of the alternative renin angiotensin (RAS) enzyme angiotensin-converting enzyme 2 (ACE2) has therapeutic potential for mitigating multi-organ radiation injury, including GI acute radiation syndrome (GI-ARS). Here, we evaluated whether pharmacologic activation of ACE2 mitigates GI-ARS in rodent models and protects against DEARE in GI-ARS survivors. 6 mice underwent radiation with sacrifice at post-radiation day 5. Single cell RNA seq was then performed from jejunum.