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Coronary Microembolization Induces Cardiomyocyte Apoptosis Through the LOX-1– Dependent Endoplasmic Reticulum Stress Pathway Involving JNK/P38 MAPK  Tao.

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Presentation on theme: "Coronary Microembolization Induces Cardiomyocyte Apoptosis Through the LOX-1– Dependent Endoplasmic Reticulum Stress Pathway Involving JNK/P38 MAPK  Tao."— Presentation transcript:

1 Coronary Microembolization Induces Cardiomyocyte Apoptosis Through the LOX-1– Dependent Endoplasmic Reticulum Stress Pathway Involving JNK/P38 MAPK  Tao Liu, MD, You Zhou, MD, Yang-Chun Liu, MD, Jiang-You Wang, MD, Qiang Su, MD, Zhong-Li Tang, MD, Lang Li, PhD  Canadian Journal of Cardiology  Volume 31, Issue 10, Pages (October 2015) DOI: /j.cjca Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

2 Figure 1 Expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) after coronary microembolization (CME). (A) LOX-1 Western blots. (B) LOX-1 band intensity normalized to glyceraldehyde 3-phosphate dehydrogenase (GAPDH); mean ± standard deviation. LOX-1 small interfering RNA (siRNA) pretreatment inhibited LOX-1 upregulation by CME, whereas the control siRNA had no effect; n = 5 for each group (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

3 Figure 2 Microinfarct area and serum c-troponin I level were increased after coronary microembolization (CME). (A) Microinfarct was not observed in the sham group but was seen in other groups subjected to CME; mean ± standard deviation. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) small interfering RNA (siRNA) reduced the microinfarct area despite CME, whereas the control siRNA showed no effect. (B) Serum c-troponin I was significantly enhanced in the CME and control siRNA groups vs the sham group; mean ± standard deviation. LOX-1 siRNA decreased serum c-troponin I. The control siRNA had no effect; n = 5 for each group (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

4 Figure 3 Cardiomyocyte apoptosis was induced after coronary microembolization (CME). Quantitative analysis of TdT-mediated dUTP-biotin nick end labeling (TUNEL)-positive cardiomyocyte; mean ± standard deviation. Apoptosis was markedly increased in the CME group, mainly in the microinfarct and its border area but not in distant areas. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) small interfering RNA (siRNA) induced a decreased apoptotic index. The control siRNA showed no effect (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group; n = 5 for each group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

5 Figure 4 Glucose-regulated protein 78 (GRP 78), C/EBP homologous protein (CHOP), cleaved caspase-12, and cleaved caspase-3 proteins were all enhanced after coronary microembolization (CME). (A) Representative Western blots. (B-E) Expression relative to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) of (B) cleaved caspase-3, (C) Glucose-regulated protein 78 (GRP 78), (D) C/EBP homologous protein (CHOP), and (E) cleaved caspase-12 was enhanced after CME; mean ± standard deviation. Pretreatment with low-density lipoprotein receptor-1 (LOX-1) small interfering RNA (siRNA) inhibited their upregulation. The control siRNA showed no effect; n = 5 for each group (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group; c = P < 0.05 vs the LOX-1 siRNA group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

6 Figure 5 Low-density lipoprotein receptor-1 (LOX-1) small interfering RNA (siRNA) effects on c-Jun NH2-terminal protein kinase (JNK) and p38 but not extracellular signal–related protein kinases (ERK) 1 and 2 after coronary microembolization (CME). (A) Representative Western blots. (B) Phosphorylation ratios (phosphorylated vs total protein); mean ± standard deviation. The phosphorylation of JNK, p38, and ERK1/2 were all induced after CME. LOX-1 siRNA inhibited the phosphorylation of JNK and p38 but not ERK1/2. The control siRNA had no effect; n = 5 for each group (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group; c = P < 0.05 vs LOX-1 siRNA group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

7 Figure 6 Effects of c-Jun NH2-terminal protein kinase (JNK) inhibitor SP or p38 inhibitor SB on JNK and p38 after coronary microembolization (CME). (A) Representative Western blots. (B) Phosphorylation ratios (phosphorylated vs total protein); mean ± standard deviation. The phosphorylation of both JNK and p38 MAPK was low in the sham group but was significantly induced after CME. JNK inhibitor specifically attenuated the phosphorylation of JNK but not p38 mitogen-activated protein kinase (MAPK). p38 inhibitor selectively decreased the phosphorylation of p38 MAPK rather than JNK; n = 5 for each group (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

8 Figure 7 c-Jun NH2-terminal protein kinase (JNK) inhibitor or p38 inhibitor effects on the expression of glucose-regulated protein 78 (GRP 78), C/EBP homologous protein (CHOP), cleaved caspase-12, and cleaved caspase-3 proteins after coronary microembolization (CME). (A) Representative Western blots. (B-E) Expression relative to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) of (B) glucose-regulated protein 78 (GRP 78), (C) CHOP, (D) cleaved caspase-12, and (E) cleaved caspase-3 were all enhanced after CME; mean ± standard deviation. Either JNK inhibitor or p38 inhibitor significantly attenuated their upregulation; n = 5 for each group (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

9 Figure 8 c-Jun NH2-terminal protein kinase (JNK) inhibitor or p38 inhibitor effects on cardiomyocyte apoptosis after coronary microembolization (CME). Quantitative analysis of TdT-mediated dUTP-biotin nick end labeling (TUNEL)-positive cardiomyocyte. Apoptosis was negligible in the sham group but was significantly induced in the CME group, mainly in the microinfarct and its border area but not in the distant area; mean ± standard deviation. Either JNK inhibitor or p38 inhibitor markedly decreased the apoptotic index despite CME (a = P < 0.05 vs the sham group; b = P < 0.05 vs the CME group; n = 5 for each group). Canadian Journal of Cardiology  , DOI: ( /j.cjca ) Copyright © 2015 Canadian Cardiovascular Society Terms and Conditions

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