Inhibition of the Let-7 Family MicroRNAs Induces Cardioprotection Against Ischemia- Reperfusion Injury in Diabetic Rats  Juchen Li, MD, Yixing Ren, MD,

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Inhibition of the Let-7 Family MicroRNAs Induces Cardioprotection Against Ischemia- Reperfusion Injury in Diabetic Rats  Juchen Li, MD, Yixing Ren, MD, Enyi Shi, MD, PhD, Zhibin Tan, MD, Jian Xiong, MD, Lihui Yan, MD, Xiaojing Jiang, MD, PhD  The Annals of Thoracic Surgery  Volume 102, Issue 3, Pages 829-835 (September 2016) DOI: 10.1016/j.athoracsur.2016.02.016 Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions

Fig 1 Expressions of the let-7 family microRNAs in the myocardium. *p < 0.05 versus NDR group, #p < 0.05 versus DR group. (C = control vector; DR = diabetic rat; L = lentivirus vectors with let-7 antimiR; NDR = nondiabetic rat.) The Annals of Thoracic Surgery 2016 102, 829-835DOI: (10.1016/j.athoracsur.2016.02.016) Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions

Fig 2 Representative digital images of infracted tissue (pale) within the area at risk (absence of blue dye) and nonischemic zones (blue). (C = control vector; DR = diabetic rat; L = lentivirus vectors with let-7 antimiR; LY = LY294002; NDR = nondiabetic rat; Ra = rapamycin.) The Annals of Thoracic Surgery 2016 102, 829-835DOI: (10.1016/j.athoracsur.2016.02.016) Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions

Fig 3 (A) Representative Western blot images showing insulin-like growth factor-1 receptor (IGF-1R), insulin receptor (InsR), and glucose transporter type 4 (GLUT4) expressions in myocardium. Densitometric quantification of (B) IGF-1R, (C) InsR, and (D) GLUT4. *p < 0.01 versus nondiabetic rat (NDR) group. #p < 0.01 versus diabetic rat (DR) group. (C = control vector; L = lentivirus vectors with let-7 antimiR.) The Annals of Thoracic Surgery 2016 102, 829-835DOI: (10.1016/j.athoracsur.2016.02.016) Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions

Fig 4 (A) Representative Western blot showing phosphorylation of Akt (P-Akt) and phosphorylation of mammalian target of rapamycin (P-mTOR) expression in myocardium. Densitometric quantification of (B) P-Akt expression and (C) P-mTOR expression. *p < 0.01 versus nondiabetic rat (NDR) group. #p < 0.01 versus diabetic rat (DR) group; †p < 0.01 versus NDR + lentivirus vectors with let-7 antimiR (L) group. (C = control vector; GAPDH = glyceraldehyde 3-phosphate dehydrogenase; LY = LY294002; Ra = rapamycin.) The Annals of Thoracic Surgery 2016 102, 829-835DOI: (10.1016/j.athoracsur.2016.02.016) Copyright © 2016 The Society of Thoracic Surgeons Terms and Conditions