Prostaglandin E2 Protects the Heart From Ischemia-Reperfusion Injury via Its Receptor Subtype EP4 by Chun-Yang Xiao, Koh-ichi Yuhki, Akiyoshi Hara, Takayuki.

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Presentation transcript:

Prostaglandin E2 Protects the Heart From Ischemia-Reperfusion Injury via Its Receptor Subtype EP4 by Chun-Yang Xiao, Koh-ichi Yuhki, Akiyoshi Hara, Takayuki Fujino, Shuhko Kuriyama, Takehiro Yamada, Koji Takayama, Osamu Takahata, Hideji Karibe, Takanobu Taniguchi, Shuh Narumiya, and Fumitaka Ushikubi Circulation Volume 109(20):2462-2468 May 25, 2004 Copyright © American Heart Association, Inc. All rights reserved.

Figure 1. Murine ventricle expresses mRNAs for EPs Figure 1. Murine ventricle expresses mRNAs for EPs. A, RT-PCR showing expressions of mRNAs for EPs. B, Competitive RT-PCR showing expression levels of mRNAs for EP2, EP3, and EP4. n=3. Figure 1. Murine ventricle expresses mRNAs for EPs. A, RT-PCR showing expressions of mRNAs for EPs. B, Competitive RT-PCR showing expression levels of mRNAs for EP2, EP3, and EP4. n=3. Chun-Yang Xiao et al. Circulation. 2004;109:2462-2468 Copyright © American Heart Association, Inc. All rights reserved.

Figure 2. Infarct size in EP4−/− heart after I/R is larger than that in wild-type heart. Figure 2. Infarct size in EP4−/− heart after I/R is larger than that in wild-type heart. A, Representative photomicrographs of horizontal section of left ventricle from wild-type and EP4−/− mice after I/R. Tissue area stained blue represents nonischemic area. Within ischemic area, tissue area stained red is still alive, and tissue area appearing pale white is necrotic. B, Infarct size after I/R in wild-type (□) and EP4−/− (▪) mice. Infarct size and AAR as a percentage of AAR and LVS, respectively, are presented. *P<0.05 vs wild-type group. n=10. Chun-Yang Xiao et al. Circulation. 2004;109:2462-2468 Copyright © American Heart Association, Inc. All rights reserved.

Figure 3. Endogenous PGE2 exhibits cardioprotective effect against I/R injury in vitro. Figure 3. Endogenous PGE2 exhibits cardioprotective effect against I/R injury in vitro. A and B, Developed (A) and diastolic (B) tensions during reperfusion period. C, Release of CK into coronary flow during reperfusion period. D, Changes of coronary flow rate during reperfusion period. In A, B, and D, values are expressed as a percentage of respective preischemic value. ○, Wild-type hearts; •, EP4−/− hearts. *P<0.05 vs wild-type hearts. n=13. Chun-Yang Xiao et al. Circulation. 2004;109:2462-2468 Copyright © American Heart Association, Inc. All rights reserved.

Figure 4. Effects of AE1-329 on [cAMP]i in noncardiomyocytes (A) and cardiomyocytes (B). Figure 4. Effects of AE1-329 on [cAMP]i in noncardiomyocytes (A) and cardiomyocytes (B). A, Concentration-dependent stimulatory effect of AE1-329 on [cAMP]i in noncardiomyocytes from wild-type (○, n=4) and EP4−/− (•, n=3) mice. Error bars are hidden within symbols. B, Effect of AE1-329 on [cAMP]i in cardiomyocytes. Cells were incubated with vehicle (□, n=5 for wild-type group and n=4 for EP4−/− group) or 10 μmol/L of AE1-329 (▪, n=5 for wild-type group and n=4 for EP4−/− group). *P<0.05 vs control group. Chun-Yang Xiao et al. Circulation. 2004;109:2462-2468 Copyright © American Heart Association, Inc. All rights reserved.

Figure 5. An EP4 agonist decreases infarct size in vivo in wild-type but not in EP4−/− mice. Figure 5. An EP4 agonist decreases infarct size in vivo in wild-type but not in EP4−/− mice. Infarct size as a percentage of AAR is presented. □ indicates control group; , group injected with 4819-CD before ischemia; and ▪, group injected with 4819-CD after ischemia. *P<0.05 vs control group. †P<0.05 vs wild-type group. n=6 to 8. Chun-Yang Xiao et al. Circulation. 2004;109:2462-2468 Copyright © American Heart Association, Inc. All rights reserved.