Delayed effects of acute radiation exposure on the cardiovascular system using a murine model of the hematopoietic acute radiation syndrome
dc.contributor.author | Thungu, Beatrice | |
dc.contributor.author | Ortiz, Miguel | |
dc.contributor.author | Unthank, Joseph L. | |
dc.contributor.author | Orschell, Christie M. | |
dc.contributor.author | Miller, Steven J. | |
dc.date.accessioned | 2016-05-06T14:59:24Z | |
dc.date.available | 2016-05-06T14:59:24Z | |
dc.date.issued | 2016-04-08 | |
dc.description | poster abstract | en_US |
dc.description.abstract | Introduction. Exposure to high level radiation from accidents or belligerent activities results in acute and chronic organ damage. The hematopoietic system is the most sensitive organ to radiation damage (2-10 Gy) and results in the hematopoietic acute radiation syndrome (H-ARS). Survivors of H-ARS are plagued months to years later with delayed effects of acute radiation exposure (DEARE), characterized by chronic illnesses affecting multiple organ systems. Previous results using the murine H-ARS model showed numerous kidney and heart DEARErelated pathologies similar to humans, including tissue fibrosis and elevated blood urea nitrogen. The goal of this study was to utilize the murine H-ARS model to determine possible roles for abnormal iron metabolism, inflammation, oxidant stress, and senescence in the development of cardiac DEARE. Methods. Mice (C57BL/6; 12 week-old) received total body irradiation (TBI: ~8.5-8.7 Gy, 137Cs, LD50to LD70) and hearts were harvested at various times post-TBI from H-ARS survivors. Paraffin tissue sections were stained with hematoxylin/eosin or Perls Prussian Blue, or reacted with a macrophage-specific antibody (F4/80). Total RNA was purified from fresh tissue and changes in mRNA expression were assessed by real-time PCR for the senescence marker p16 and NADPH oxidase subunits Nox2, Nox4, or p47phox. Results/Significance. Compared to age-matched non-irradiated controls (NI), tissue iron deposits were increased in irradiated (IR) hearts at 4 months, and progressively declined with time post-TBI. Numbers of macrophages were greater in IR vs. NI sections at all time points and decreased with time post-TBI. Nox2 and Nox4 mRNA expression was increased at both 9 and 21 months post-TBI, but p47phox increased only at 21 months. Expression of p16 in IR heart was increased at 7, but not at 22 months post-TBI. Taken together, the results indicate abnormal iron metabolism, inflammation, oxidant stress, and early senescence may contribute to development of cardiac DEARE. | en_US |
dc.identifier.citation | Beatrice Thungu, Miguel Ortiz, Joseph L. Unthank, Christie M. Orschell, and Steven J. Miller. 2016 April 8. Delayed effects of acute radiation exposure on the cardiovascular system using a murine model of the hematopoietic acute radiation syndrome. Poster session presented at IUPUI Research Day 2016, Indianapolis, Indiana. | en_US |
dc.identifier.uri | https://hdl.handle.net/1805/9541 | |
dc.language.iso | en_US | en_US |
dc.publisher | Office of the Vice Chancellor for Research | en_US |
dc.subject | acute radiation exposure | en_US |
dc.subject | cardiovascular system | en_US |
dc.subject | hematopoietic acute radiation syndrome (H-ARS) | en_US |
dc.subject | organ damage | en_US |
dc.title | Delayed effects of acute radiation exposure on the cardiovascular system using a murine model of the hematopoietic acute radiation syndrome | en_US |
dc.type | Poster | en_US |
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