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On-line Access: 2013-07-30

Received: 2013-06-18

Revision Accepted: 2013-07-05

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Journal of Zhejiang University SCIENCE B 2013 Vol.14 No.8 P.664-669

http://doi.org/10.1631/jzus.BQICC701


Interleukin-17 and acute coronary syndrome


Author(s):  Sheng-an Su, Hong Ma, Li Shen, Mei-xiang Xiang, Jian-an Wang

Affiliation(s):  Cardiovascular Key Lab of Zhejiang Province, Department of Cardiology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China

Corresponding email(s):   xiangmx@yahoo.com

Key Words:  Interleukin-17, Acute coronary syndrome, Atherosclerosis, Inflammation


Sheng-an Su, Hong Ma, Li Shen, Mei-xiang Xiang, Jian-an Wang. Interleukin-17 and acute coronary syndrome[J]. Journal of Zhejiang University Science B, 2013, 14(8): 664-669.

@article{title="Interleukin-17 and acute coronary syndrome",
author="Sheng-an Su, Hong Ma, Li Shen, Mei-xiang Xiang, Jian-an Wang",
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year="2013",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.BQICC701"
}

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%T Interleukin-17 and acute coronary syndrome
%A Sheng-an Su
%A Hong Ma
%A Li Shen
%A Mei-xiang Xiang
%A Jian-an Wang
%J Journal of Zhejiang University SCIENCE B
%V 14
%N 8
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%@ 1673-1581
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.BQICC701

TY - JOUR
T1 - Interleukin-17 and acute coronary syndrome
A1 - Sheng-an Su
A1 - Hong Ma
A1 - Li Shen
A1 - Mei-xiang Xiang
A1 - Jian-an Wang
J0 - Journal of Zhejiang University Science B
VL - 14
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SP - 664
EP - 669
%@ 1673-1581
Y1 - 2013
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.BQICC701


Abstract: 
inflammation plays an important role in atherosclerosis, which is also crucial for acute coronary syndrome (ACS). Recent studies have revealed that interleukin (IL)-17, which was regarded as a pro-inflammatory cytokine, has a dual function in the progress of ACS. In this review, we sum up both experimental and clinical studies on the relevance of IL-17 to atherosclerosis and its complications, and summarize the research progress on the effect of IL-17 on the atherosclerotic plaque stability and ACS onset. Although the studies are controversial and the mechanism remains unclear, we highlight the knowledge of the role of IL-17 in ACS and elucidate its potential mechanism.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Ávalos, A.M., Apablaza, F.A., Quiroz, M., Toledo, V., Peño, J.P., Michea, L., Irarrázabal, C.E., Carrión, F.A., Figueroa, F.E., 2012. IL-17A levels increase in the infarcted region of the left ventricle in a rat model of myocardial infarction. Biol. Res., 45(2):193-200.

[2]Baldeviano, G.C., Barin, J.G., Talor, M.V., Srinivasan, S., Bedja, D., Zheng, D., Gabrielson, K., Iwakura, Y., Rose, N.R., Cihakova, D., 2010. Interleukin-17A is dispensable for myocarditis but essential for the progression to dilated cardiomyopathy. Circ. Res., 106(10):1646-1655.

[3]Binder, C.J., Chang, M.K., Shaw, P.X., Miller, Y.I., Hartvigsen, K., Dewan, A., Witztum, J.L., 2002. Innate and acquired immunity in atherogenesis. Nat. Med., 8(11):1218-1226.

[4]Chang, S.H., Dong, C., 2007. A novel heterodimeric cytokine consisting of IL-17 and IL-17F regulates inflammatory responses. Cell Res., 17(5):435-440.

[5]Chen, S., Crother, T.R., Arditi, M., 2010a. Emerging role of IL-17 in atherosclerosis. J. Innate Immun., 2(4):325-333.

[6]Chen, S., Shimada, K., Zhang, W., Huang, G., Crother, T.R., Arditi, M., 2010b. IL-17A is proatherogenic in high-fat diet-induced and chlamydia pneumoniae infection-accelerated atherosclerosis in mice. J. Immunol., 185(9):5619-5627.

[7]Cheng, X., Yu, X., Ding, Y., Fu, Q., Xie, J., Tang, T., Yao, R., Chen, Y., Liao, Y., 2008. The Th17/Treg imbalance in patients with acute coronary syndrome. Clin. Immunol., 127(1):89-97.

[8]Crea, F., Liuzzo, G., 2013. Pathogenesis of acute coronary syndromes. J. Am. Coll. Cardiol., 61(1):1-11.

[9]Cybulsky, M.I., Gimbrone, M.A.Jr., 1991. Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science, 251(4995):788-791.

[10]Danzaki, K., Matsui, Y., Ikesue, M., Ohta, D., Ito, K., Kanayama, M., Kurotaki, D., Morimoto, J., Iwakura, Y., Yagita, H., et al., 2012. Interleukin-17A deficiency accelerates unstable atherosclerotic plaque formation in apolipoprotein E-deficient mice. Arterioscler. Thromb. Vasc. Biol., 32(2):273-280.

[11]de Boer, O.J., van der Meer, J.J., Teeling, P., van der Loos, C.M., Idu, M.M., van Maldegem, F., Aten, J., van der Wal, A.C., 2010. Differential expression of interleukin-17 family cytokines in intact and complicated human atherosclerotic plaques. J. Pathol., 220(4):499-508.

[12]de Boer, O.J., Li, X., Teeling, P., Mackaay, C., Ploegmakers, H.J., van der Loos, C.M., Daemen, M.J., de Winter, R.J., van der Wal, A.C., 2013. Neutrophils, neutrophil extracellular traps and interleukin-17 associate with the organisation of thrombi in acute myocardial infarction. Thromb. Haemost., 109(2):290-297.

[13]Ding, H., Yang, J., Yang, J., Ding, J., Chen, P., Zhu, P., 2012. Interleukin-17 contributes to cardiovascular diseases. Mol. Biol. Rep., 39(7):7473-7478.

[14]Drakopoulou, M., Toutouzas, K., Stefanadi, E., Tsiamis, E., Tousoulis, D., Stefanadis, C., 2009. Association of inflammatory markers with angiographic severity and extent of coronary artery disease. Atherosclerosis, 206(2):335-339.

[15]Edfeldt, K., Swedenborg, J., Hansson, G.K., Yan, Z.Q., 2002. Expression of Toll-like receptors in human atherosclerotic lesions: a possible pathway for plaque activation. Circulation, 105(10):1158-1161.

[16]Eid, R.E., Rao, D.A., Zhou, J., Lo, S.F., Ranjbaran, H., Gallo, A., Sokol, S.I., Pfau, S., Pober, J.S., Tellides, G., 2009. Interleukin-17 and interferon-γ are produced concomitantly by human coronary artery-infiltrating T cells and act synergistically on vascular smooth muscle cells. Circulation, 119(10):1424-1432.

[17]Erbel, C., Chen, L., Bea, F., Wangler, S., Celik, S., Lasitschka, F., Wang, Y., Boeckler, D., Katus, H.A., Dengler, T.J., 2009. Inhibition of IL-17A attenuates atherosclerotic lesion development in ApoE-deficient mice. J. Immunol., 183(12):8167-8175.

[18]Gaffen, S.L., 2009. Structure and signalling in the IL-17 receptor family. Nat. Rev. Immunol., 9(8):556-567.

[19]Griffiths, C.E., Strober, B.E., van de Kerkhof, P., Ho, V., Fidelus-Gort, R., Yeilding, N., Guzzo, C., Xia, Y., Zhou, B., Li, S., et al., 2010. Comparison of ustekinumab and etanercept for moderate-to-severe psoriasis. N. Engl. J. Med., 362(2):118-128.

[20]Hansson, G.K., 2005. Inflammation, atherosclerosis, and coronary artery disease. N. Engl. J. Med., 352(16):1685-1695.

[21]Harrington, L.E., Hatton, R.D., Mangan, P.R., Turner, H., Murphy, T.L., Murphy, K.M., Weaver, C.T., 2005. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat. Immunol., 6(11):1123-1132.

[22]Hashmi, S., Zeng, Q.T., 2006. Role of interleukin-17 and interieukin-17-induced cytokines interleukin-6 and interleukin-8 in unstable coronary artery disease. Coron. Artery Dis., 17(8):699-706.

[23]Houtkamp, M.A., van der Wal, A.C., de Boer, O.J., van der Loos, C.M., de Boer, P.A., Moorman, A.F., Becker, A.E., 2001. Interleukin-15 expression in atherosclerotic plaques: an alternative pathway for T-cell activation in atherosclerosis? Arterioscler. Thromb. Vasc. Biol., 21(7):1208-1213.

[24]Iwakura, Y., Ishigame, H., Saijo, S., Nakae, S., 2011. Functional specialization of interleukin-17 family members. Immunity, 34(2):149-162.

[25]Jafarzadeh, A., Esmaeeli-Nadimi, A., Nough, H., Nemati, M., Rezayati, M.T., 2009. Serum levels of interleukin (IL)-13, IL-17 and IL-18 in patients with ischemic heart disease. Anadolu Kardiyol. Derg., 9(2):75-83.

[26]Kolls, J.K., Linden, A., 2004. Interleukin-17 family members and inflammation. Immunity, 21(4):467-476.

[27]Liao, Y.H., Xia, N., Zhou, S.F., Tang, T.T., Yan, X.X., Lv, B.J., Nie, S.F., Wang, J., Iwakura, Y., Xiao, H., et al., 2012. Interleukin-17A contributes to myocardial ischemia/ reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration. J. Am. Coll. Cardiol., 59(4):420-429.

[28]Libby, P., 2013. Mechanisms of acute coronary syndromes and their implications for therapy. N. Engl. J. Med., 368(21):2004-2013.

[29]Libby, P., Ridker, P.M., Maseri, A., 2002. Inflammation and atherosclerosis. Circulation, 105(9):1135-1143.

[30]Lichtman, A.H., Binder, C.J., Tsimikas, S., Witztum, J.L., 2013. Adaptive immunity in atherogenesis: new insights and therapeutic approaches. J. Clin. Invest., 123(1):27-36.

[31]Liu, L., Zhu, Y., Chen, Z., Chen, Z., Zeng, Q., Liu, X., Zhang, Q., Qian, C., Du Y.M., Zhao, N., 2012. Expression of interleukin-17 in the myocardium of rats with myocardial infarction. Chin. J. Tissue Eng. Res., 16:1985-1988 (in Chinese).

[32]Lopez-Pedrera, C., Perez-Sanchez, C., Ramos-Casals, M., Santos-Gonzalez, M., Rodriguez-Ariza, A., Cuadrado, M.J., 2012. Cardiovascular risk in systemic autoimmune diseases: epigenetic mechanisms of immune regulatory functions. Clin. Dev. Immunol., 2012:974648.

[33]Maione, F., Cicala, C., Liverani, E., Mascolo, N., Perretti, M., D′Acquisto, F., 2011. IL-17A increases ADP-induced platelet aggregation. Biochem. Biophys. Res. Commun., 408(4):658-662.

[34]Nakashima, Y., Raines, E.W., Plump, A.S., Breslow, J.L., Ross, R., 1998. Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse. Arterioscler. Thromb. Vasc. Biol., 18(5):842-851.

[35]Patel, K.D., Murphy, R.T., White, M., Gasparro, D., Kelleher, D.P., Ryan, T., McManus, R., Ryan, A.W., 2009. Interleukin 17: an unlikely marker of acute coronary syndrome? Atherosclerosis, 205(1):33-34.

[36]Romain, M., Taleb, S., Dalloz, M., Ponnuswamy, P., Esposito, B., Perez, N., Wang, Y., Yoshimura, A., Tedgui, A., Mallat, Z., 2013. Overexpression of SOCS3 in T lymphocytes leads to impaired interleukin-17 production and severe aortic aneurysm formation in mice—brief report. Arterioscler. Thromb. Vasc. Biol., 33(3):581-584.

[37]Simon, T., Taleb, S., Danchin, N., Laurans, L., Rousseau, B., Cattan, S., Montely, J., Dubourg, O., Tedgui, A., Kotti, S., et al., 2013. Circulating levels of interleukin-17 and cardiovascular outcomes in patients with acute myocardial infarction. Eur. Heart J., 34(8):570-577.

[38]Smith, E., Prasad, K.M., Butcher, M., Dobrian, A., Kolls, J.K., Ley, K., Galkina, E., 2010. Blockade of interleukin-17A results in reduced atherosclerosis in apolipoprotein E-deficient mice. Circulation, 121(15):1746-1755.

[39]Taleb, S., Romain, M., Ramkhelawon, B., Uyttenhove, C., Pasterkamp, G., Herbin, O., Esposito, B., Perez, N., Yasukawa, H., van Snick, J., et al., 2009. Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis. J. Exp. Med., 206(10):2067-2077.

[40]Troitskaya, M., Baysa, A., Vaage, J., Sand, K.L., Maghazachi, A.A., Valen, G., 2012. Interleukin-17 (IL-17) expression is reduced during acute myocardial infarction: role on chemokine receptor expression in monocytes and their in vitro chemotaxis towards chemokines. Toxins, 4(12):1427-1439.

[41]Valente, A.J., Yoshida, T., Gardner, J.D., Somanna, N., Delafontaine, P., Chandrasekar, B., 2012. Interleukin-17A stimulates cardiac fibroblast proliferation and migration via negative regulation of the dual-specificity phosphatase MKP-1/DUSP-1. Cell Signal, 24(2):560-568.

[42]van Es, T., van Puijvelde, G.H.M., Ramos, O.H., Segers, F.M.E., Joosten, L.A., van den Berg, W.B., Michon, I.M., de Vos, P., van Berkel, Th.J.C., Kuiper, J., 2009. Attenuated atherosclerosis upon IL-17R signaling disruption in LDLr deficient mice. Biochem. Biophys. Res. Commun., 388(2):261-265.

[43]Xie, J., Wang, J., Tang, T., Chen, J., Gao, X., Yuan, J., Zhou, Z., Liao, M., Yao, R., Yu, X., et al., 2010. The Th17/Treg functional imbalance during atherogenesis in ApoE−/− mice. Cytokine, 49(2):185-193.

[44]Yamashita, T., Obana, M., Hayama, A., Iwakura, T., Komuro, I., Nakayama, H., Fujio, Y., 2011. Th17 cells exhibit protective effects against cardiac fibrosis after myocardial infarction. Circulation, 124:A14566.

[45]Yan, X., Sano, M., Shichita, T., Matsuhashi, T., Katsumata, Y., Yoshimura, A., Fukuda, K., 2011. Deleterious effect of interleukin-23/interleukin-17 axis and γδT cells in left ventricular remodeling after myocardial infarction. Circulation, 124:A14614.

[46]Zhang, S., Yuan, J., Yu, M., Fan, H., Guo, Z., Yang, R., Guo, H., Liao, Y., Wang, M., 2012. IL-17A facilitates platelet function through the ERK2 signaling pathway in patients with acute coronary syndrome. PLoS One, 7(7):e40641.

[47]Zhu, S., Qian, Y., 2012. IL-17/IL-17 receptor system in autoimmune disease: mechanisms and therapeutic potential. Clin. Sci. (Lond.), 122(11):487-511.

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