p53 Functions in Endothelial Cells to Prevent Radiation-Induced Myocardial Injury in Mice

Chang-Lung Lee, Everett J. Moding, Kyle C. Cuneo, Yifan Li, Julie M. Sullivan, Lan Mao, Iman Washington, Laura B. Jeffords, Rafaela C. Rodrigues, Yan Ma, Shiva Das, Christopher D. Kontos, Yongbaek Kim, Howard A. Rockman, David G. Kirsch*

*To whom correspondence should be addressed. E-mail: david.kirsch{at}duke.edu

This PDF file includes:

• Fig. S1. In Tie2Cre mice, Cre is expressed specifically in endothelial cells compared to cardiomyocytes.
• Fig. S2. Pericardial disease in Tie2Cre; p53^FL/– mice after 12 Gy whole-heart irradiation.
• Fig. S3. Increased TUNEL-positive myocardial capillaries in Tie2Cre; p53^FL/– mice 4 weeks after 12 Gy whole-heart irradiation.
• Fig. S4. Tie2Cre; p53^FL/– mice show increased vascular permeability of myocardial capillaries 4 weeks after 12 Gy whole-heart irradiation.
• Fig. S5. A small subset of hematopoietic cells expresses VECre.
• Fig. S6. In VECre mice, Cre is specifically expressed in a subset of endothelial cells in the myocardium.
• Fig. S7. Characterization of cardiac endothelial cells cultured in vitro.
• Fig. S8. p21 functions downstream of p53 to regulate radiation response in cardiac endothelial cells.
• Table S1. Serial echocardiographic measurements in Tie2Cre; p53^FL/+ and Tie2Cre; p53^FL/– mice before and after 12 Gy whole-heart irradiation.
• Table S2. Serial echocardiographic measurements in p21^+/– and p21^–/– mice before and after 12 Gy whole-heart irradiation.
  

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© 2012 American Association for the Advancement of Science