The mechanisms of inflammation and apoptosis in myocardial infarction

JIANG Shu; RUI Yaocheng; Li Tiejun

doi:10.3969/j.issn.1006-0111.2016.02.007

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Article Navigation > Journal of Pharmaceutical Practice and Service > 2016 > 34(2): 119-123

JIANG Shu, RUI Yaocheng, Li Tiejun. The mechanisms of inflammation and apoptosis in myocardial infarction[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007

Citation:

JIANG Shu, RUI Yaocheng, Li Tiejun. The mechanisms of inflammation and apoptosis in myocardial infarction[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(2): 119-123. doi: 10.3969/j.issn.1006-0111.2016.02.007

The mechanisms of inflammation and apoptosis in myocardial infarction

doi: 10.3969/j.issn.1006-0111.2016.02.007

Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China

Received Date: 2014-03-13
Rev Recd Date: 2015-06-01

Abstract

The inflammation and apoptosis were vital important in the progress and recovery in myocardial infarction. Apoptosis was regulated by inflammation though TNF-α, CHOP, IL-10 and α7nAChR signal pathways and influenced the severity of the inflammation via feedback regulation. Inflammation and apoptosis affected myocardial infarction size and cardiac function recovery together. Inhibition of inflammation, reducing apoptosis had been proved to be the important parts in prevention of ventricular remodeling and regulating cardiac dysfunction after myocardial infarction, which had broad prospects.
- myocardial infarction,
- inflammation,
- apoptosis

References

[1]	Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats[J]. Lab Invest, 1996, 74(1):86-107.
[2]	Roy S, Khanna S, Kuhn DE, et al. Transcriptome analysis of the ischemia-reperfused remodeling myocardium:temporal changes in inflammation and extracellular matrix[J]. Physiol Genom, 2006, 25(3):364-374.
[3]	van den Akker F, Deddens JC, Doevendans PA, et al. Cardiac stem cell therapy to modulate inflammation upon myocardial infarction[J]. Biochem Biophys Acta, 2013, 1830(2):2449-2458.
[4]	Arslan F, de Kleijn DP, Pasterkamp G. Innate immune signaling in cardiac ischemia[J]. Nat Rev Cardiol, 2011,8(5):292-300.
[5]	Chen C, Feng Y, Zou L, et al. Role of extracellular RNA and TLR3-Trif signaling in myocardial ischemia-reperfusion injury[J]. J Am Heart Assoc, 2014, 3(1):e000683.
[6]	Liehn EA, Merx MW, Postea O, et al. Ccr1 deficiency reduces inflammatory remodelling and preserves left ventricular function after myocardial infarction[J]. J Cell Mol Med, 2008, 12(2):496-506.
[7]	Chello M, Anselmi A, Spadaccio C, et al. Simvastatin increases neutrophil apoptosis and reduces inflammatory reaction after coronary surgery[J]. Ann Thorac Surg, 2007, 83(4):1374-1380.
[8]	Buyukkaya E, Poyraz F, Karakas MF, et al. Usefulness of monocyte chemoattractant protein-1 to predict no-reflow and three-year mortality in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention[J]. Am J Cardiol, 2013, 112(2):187-193.
[9]	Dong F, Harvey J, Finan A, et al. Myocardial CXCR4 expression is required for mesenchymal stem cell mediated repair following acute myocardial infarction[J]. Circulation, 2012, 126(3):314-324.
[10]	Miller EJ, Li J, Leng L, et al. Macrophage migration inhibitory factor stimulates AMP-activated protein kinase in the ischaemic heart[J]. Nature, 2008, 451(7178):578-582.
[11]	Gao XM, Liu Y, White D, et al. Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia-reperfusion injury:a predominant role of anti-inflammation[J]. J Mol Cell Cardiol, 2011, 50(6):991-999.
[12]	Bradley JR. TNF-mediated inflammatory disease[J]. J Pathol, 2008, 214(2):149-160.
[13]	Peter ME, Krammer PH. The CD95(APO-1/Fas) DISC and beyond[J]. Cell Death Differ, 2003, 10(1):26-35.
[14]	Zhang R, Xu Y, Ekman N, et al. Etk/Bmx transactivates vascular endothelial growth factor 2 and recruits phosphatidylinositol 3-kinase to mediate the tumor necrosis factor-induced angiogenic pathway[J]. J Biol Chem, 2003,278(51):51267-51276.
[15]	Miyazaki Y, Kaikita K, Endo M, et al. C/EBP homologous protein deficiency attenuates myocardial reperfusion injury by inhibiting myocardial apoptosis and inflammation[J]. Arterioscler Thromb Vasc Biol, 2011, 31(5):1124-1132.
[16]	Oyadomari S, Mori M. Roles of CHOP/GADD153 in endoplasmic reticulum stress[J]. Cell Death Differ, 2004, 11(4):381-389.
[17]	Li Y, Schwabe RF, DeVries-Seimon T, et al. Free cholesterol-loaded macrophages are an abundant source of tumor necrosis factor-a and interleukin-6:model of NF-kappaB-and map kinase-dependent inflammation in advanced atherosclerosis[J]. J Biol Chem, 2005, 280(23):21763-21772.
[18]	Krishnamurthy P, Lambers E, Verma S, et al. Myocardial knockdown of mRNA-stabilizing protein HuR attenuates post-MI inflammatory response and left ventricular dysfunction in IL-10-null mice[J]. FASEB J, 2010, 24(7):2484-2494.
[19]	Krishnamurthy P, Rajasingh J, Lambers E, et al. IL-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR[J]. Circ Res, 2009, 104(2):e9-18.
[20]	Zhao M, He X, Bi XY, et al. Vagal stimulation triggers peripheral vascular protection through the cholinergic anti-inflammatory pathway in a rat model of myocardial ischemia/reperfusion[J]. Basic Res Cardiol, 2013, 108(3):345.
[21]	Kakinuma Y, Ando M, Kuwabara M, et al. Acetylcholine from vagal stimulation protects cardiomyocytes against ischemia and hypoxia involving additive non-hypoxic induction of HIF-1alpha[J]. FEBS Lett, 2005, 579(10):2111-2118.
[22]	Ottani A, Giuliani D, Galantucci M, et al. Melanocortins counteract inflammatory and apoptotic responses to prolonged myocardial ischemia/reperfusion through a vagus nerve-mediated mechanism[J]. Eur J Pharmacol, 2010, 637(1-3):124-130.
[23]	Takai S, Jin D, Miyazaki M. Multiple mechanisms for the action of chymase inhibitors[J]. J Pharmacol Sci, 2012, 118(3):311-316.
[24]	Oyamada S, Bianchi C, Takai S, et al. Chymase inhibition reduces infarction and matrix metalloproteinase-9 activation and attenuates inflammation and fibrosis after acute myocardial ischemia/reperfusion[J]. J Pharmacol Exp Ther, 2011, 339(1):143-151.
[25]	Chao J, Chao L. Kallikrein-kinin in stroke, cardiovascular and renal disease[J]. Exp Physiol, 2005, 90(3):291-298.
[26]	Chao J, Yin H, Gao L, et al. Tissue kallikrein elicits cardioprotection by direct kinin b2 receptor activation independent of kinin formation[J]. Hypertension, 2008, 52(4):715-720.
[27]	Stadnicki A. Intestinal tissue kallikrein-kinin system in inflammatory bowel disease[J]. Inflamm Bowel Dis, 2011, 17(2):645-654.
[28]	Yao YY, Yin H, Shen B, et al. Tissue kallikrein infusion prevents cardiomyocyte apoptosis, inflammation and ventricular remodeling after myocardial infarction[J]. Regul Pept, 2007, 140(1-2):12-20.
[29]	Rodrigo R, Prieto JC, Castillo R. Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n-3 fatty acids:molecular mechanisms and potential clinical applications[J]. Clin Sci, 2013, 124(1):1-15.
[30]	Oropeza M, Petersen B, Carnwath JW, et al. Transgenic expression of the human A20 gene in cloned pigs provides protection against apoptotic and inflammatory stimuli[J]. Xenotransplantation, 2009, 16(6):522-534.
[31]	Hunt DL, Campbell PH, Zambon AC, et al. Early postmyocardial infarction survival in Murphy Roths Large mice is mediated by attenuated apoptosis and inflammation but depends on genetic background[J]. Exp Physiol, 2012, 97(1):102-114.
[32]	Meybohm P, Gruenewald M, Albrecht M, et al. Hypothermia and postconditioning after cardiopulmonary resuscitation reduce cardiac dysfunction by modulating inflammation, apoptosis and remodeling[J]. PLoS ONE, 2009, 4(10):e7588.
[33]	Diepenhorst GM, Ciurana CL, Diaz Padilla N, et al. IgM antibodies against apoptotic cells and phosphorylcholine in patients with acute myocardial infarction in relation to infarct size and inflammatory response[J]. Adv Clin Exp Med, 2012, 21(4):455-467.
[34]	Vincent A, Lattuca B, Merlet N, et al. New insights in research about acute ischemic myocardial injury and inflammation[J]. Antiinfl Antialler Agents Med Chem, 2013, 12(1):47-54.

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通讯作者: 陈斌, [email protected]

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沈阳化工大学材料科学与工程学院沈阳 110142

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The mechanisms of inflammation and apoptosis in myocardial infarction

Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China

Received Date: 2014-03-13

Rev Recd Date: 2015-06-01

Key words:

Abstract: The inflammation and apoptosis were vital important in the progress and recovery in myocardial infarction. Apoptosis was regulated by inflammation though TNF-α, CHOP, IL-10 and α7nAChR signal pathways and influenced the severity of the inflammation via feedback regulation. Inflammation and apoptosis affected myocardial infarction size and cardiac function recovery together. Inhibition of inflammation, reducing apoptosis had been proved to be the important parts in prevention of ventricular remodeling and regulating cardiac dysfunction after myocardial infarction, which had broad prospects.

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Reference (34)

[1]	Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats[J]. Lab Invest, 1996, 74(1):86-107.
[2]	Roy S, Khanna S, Kuhn DE, et al. Transcriptome analysis of the ischemia-reperfused remodeling myocardium:temporal changes in inflammation and extracellular matrix[J]. Physiol Genom, 2006, 25(3):364-374.
[3]	van den Akker F, Deddens JC, Doevendans PA, et al. Cardiac stem cell therapy to modulate inflammation upon myocardial infarction[J]. Biochem Biophys Acta, 2013, 1830(2):2449-2458.
[4]	Arslan F, de Kleijn DP, Pasterkamp G. Innate immune signaling in cardiac ischemia[J]. Nat Rev Cardiol, 2011,8(5):292-300.
[5]	Chen C, Feng Y, Zou L, et al. Role of extracellular RNA and TLR3-Trif signaling in myocardial ischemia-reperfusion injury[J]. J Am Heart Assoc, 2014, 3(1):e000683.
[6]	Liehn EA, Merx MW, Postea O, et al. Ccr1 deficiency reduces inflammatory remodelling and preserves left ventricular function after myocardial infarction[J]. J Cell Mol Med, 2008, 12(2):496-506.
[7]	Chello M, Anselmi A, Spadaccio C, et al. Simvastatin increases neutrophil apoptosis and reduces inflammatory reaction after coronary surgery[J]. Ann Thorac Surg, 2007, 83(4):1374-1380.
[8]	Buyukkaya E, Poyraz F, Karakas MF, et al. Usefulness of monocyte chemoattractant protein-1 to predict no-reflow and three-year mortality in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention[J]. Am J Cardiol, 2013, 112(2):187-193.
[9]	Dong F, Harvey J, Finan A, et al. Myocardial CXCR4 expression is required for mesenchymal stem cell mediated repair following acute myocardial infarction[J]. Circulation, 2012, 126(3):314-324.
[10]	Miller EJ, Li J, Leng L, et al. Macrophage migration inhibitory factor stimulates AMP-activated protein kinase in the ischaemic heart[J]. Nature, 2008, 451(7178):578-582.
[11]	Gao XM, Liu Y, White D, et al. Deletion of macrophage migration inhibitory factor protects the heart from severe ischemia-reperfusion injury:a predominant role of anti-inflammation[J]. J Mol Cell Cardiol, 2011, 50(6):991-999.
[12]	Bradley JR. TNF-mediated inflammatory disease[J]. J Pathol, 2008, 214(2):149-160.
[13]	Peter ME, Krammer PH. The CD95(APO-1/Fas) DISC and beyond[J]. Cell Death Differ, 2003, 10(1):26-35.
[14]	Zhang R, Xu Y, Ekman N, et al. Etk/Bmx transactivates vascular endothelial growth factor 2 and recruits phosphatidylinositol 3-kinase to mediate the tumor necrosis factor-induced angiogenic pathway[J]. J Biol Chem, 2003,278(51):51267-51276.
[15]	Miyazaki Y, Kaikita K, Endo M, et al. C/EBP homologous protein deficiency attenuates myocardial reperfusion injury by inhibiting myocardial apoptosis and inflammation[J]. Arterioscler Thromb Vasc Biol, 2011, 31(5):1124-1132.
[16]	Oyadomari S, Mori M. Roles of CHOP/GADD153 in endoplasmic reticulum stress[J]. Cell Death Differ, 2004, 11(4):381-389.
[17]	Li Y, Schwabe RF, DeVries-Seimon T, et al. Free cholesterol-loaded macrophages are an abundant source of tumor necrosis factor-a and interleukin-6:model of NF-kappaB-and map kinase-dependent inflammation in advanced atherosclerosis[J]. J Biol Chem, 2005, 280(23):21763-21772.
[18]	Krishnamurthy P, Lambers E, Verma S, et al. Myocardial knockdown of mRNA-stabilizing protein HuR attenuates post-MI inflammatory response and left ventricular dysfunction in IL-10-null mice[J]. FASEB J, 2010, 24(7):2484-2494.
[19]	Krishnamurthy P, Rajasingh J, Lambers E, et al. IL-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR[J]. Circ Res, 2009, 104(2):e9-18.
[20]	Zhao M, He X, Bi XY, et al. Vagal stimulation triggers peripheral vascular protection through the cholinergic anti-inflammatory pathway in a rat model of myocardial ischemia/reperfusion[J]. Basic Res Cardiol, 2013, 108(3):345.
[21]	Kakinuma Y, Ando M, Kuwabara M, et al. Acetylcholine from vagal stimulation protects cardiomyocytes against ischemia and hypoxia involving additive non-hypoxic induction of HIF-1alpha[J]. FEBS Lett, 2005, 579(10):2111-2118.
[22]	Ottani A, Giuliani D, Galantucci M, et al. Melanocortins counteract inflammatory and apoptotic responses to prolonged myocardial ischemia/reperfusion through a vagus nerve-mediated mechanism[J]. Eur J Pharmacol, 2010, 637(1-3):124-130.
[23]	Takai S, Jin D, Miyazaki M. Multiple mechanisms for the action of chymase inhibitors[J]. J Pharmacol Sci, 2012, 118(3):311-316.
[24]	Oyamada S, Bianchi C, Takai S, et al. Chymase inhibition reduces infarction and matrix metalloproteinase-9 activation and attenuates inflammation and fibrosis after acute myocardial ischemia/reperfusion[J]. J Pharmacol Exp Ther, 2011, 339(1):143-151.
[25]	Chao J, Chao L. Kallikrein-kinin in stroke, cardiovascular and renal disease[J]. Exp Physiol, 2005, 90(3):291-298.
[26]	Chao J, Yin H, Gao L, et al. Tissue kallikrein elicits cardioprotection by direct kinin b2 receptor activation independent of kinin formation[J]. Hypertension, 2008, 52(4):715-720.
[27]	Stadnicki A. Intestinal tissue kallikrein-kinin system in inflammatory bowel disease[J]. Inflamm Bowel Dis, 2011, 17(2):645-654.
[28]	Yao YY, Yin H, Shen B, et al. Tissue kallikrein infusion prevents cardiomyocyte apoptosis, inflammation and ventricular remodeling after myocardial infarction[J]. Regul Pept, 2007, 140(1-2):12-20.
[29]	Rodrigo R, Prieto JC, Castillo R. Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n-3 fatty acids:molecular mechanisms and potential clinical applications[J]. Clin Sci, 2013, 124(1):1-15.
[30]	Oropeza M, Petersen B, Carnwath JW, et al. Transgenic expression of the human A20 gene in cloned pigs provides protection against apoptotic and inflammatory stimuli[J]. Xenotransplantation, 2009, 16(6):522-534.
[31]	Hunt DL, Campbell PH, Zambon AC, et al. Early postmyocardial infarction survival in Murphy Roths Large mice is mediated by attenuated apoptosis and inflammation but depends on genetic background[J]. Exp Physiol, 2012, 97(1):102-114.
[32]	Meybohm P, Gruenewald M, Albrecht M, et al. Hypothermia and postconditioning after cardiopulmonary resuscitation reduce cardiac dysfunction by modulating inflammation, apoptosis and remodeling[J]. PLoS ONE, 2009, 4(10):e7588.
[33]	Diepenhorst GM, Ciurana CL, Diaz Padilla N, et al. IgM antibodies against apoptotic cells and phosphorylcholine in patients with acute myocardial infarction in relation to infarct size and inflammatory response[J]. Adv Clin Exp Med, 2012, 21(4):455-467.
[34]	Vincent A, Lattuca B, Merlet N, et al. New insights in research about acute ischemic myocardial injury and inflammation[J]. Antiinfl Antialler Agents Med Chem, 2013, 12(1):47-54.

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The mechanisms of inflammation and apoptosis in myocardial infarction

doi: 10.3969/j.issn.1006-0111.2016.02.007

Abstract

References

Proportional views

通讯作者: 陈斌, [email protected]

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