Interleukin-17A mediates cardiomyocyte apoptosis through Stat3-iNOS pathway

Biochimica et Biophysica Acta - Molecular Cell Research

Volumn 1863, Issue 11, 2016, Pages 2784-2794

  Su, Sheng an ^a   Yang, Du ^a   Zhu, Wei ^a   Cai, Zhejun ^a   Zhang, Na ^a   Zhao, Lina ^a   Wang, Jian an ^a   Xiang, Meixiang ^a  

^a ZHEJIANG UNIVERSITY SCHOOL OF MEDICINE   (China)

Author keywords

Apoptosis; Cardiomyocyte; iNOS; Interleukin 17A; Ischemia reperfusion injury; Stat3

Indexed keywords

INDUCIBLE NITRIC OXIDE SYNTHASE; INTERLEUKIN 17; INTERLEUKIN 17 RECEPTOR; STAT3 PROTEIN; ALPHA-CYANO-(3,4-DIHYDROXY)-N-BENZYLCINNAMIDE; IL17A PROTEIN, MOUSE; NOS2 PROTEIN, MOUSE; STAT3 PROTEIN, MOUSE; TYRPHOSTIN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CARDIAC MUSCLE CELL; CONTROLLED STUDY; ENZYME ACTIVATION; IN VIVO STUDY; MOUSE; MYOCARDIAL ISCHEMIA REPERFUSION INJURY; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN BINDING; PROTEIN EXPRESSION; ANIMAL; ANTAGONISTS AND INHIBITORS; BINDING SITE; C57BL MOUSE; CELL CULTURE; DISEASE MODEL; DRUG EFFECTS; ENZYMOLOGY; GENETIC TRANSFECTION; GENETICS; HEART INFARCTION; MALE; METABOLISM; PATHOLOGY; PHOSPHORYLATION; SIGNAL TRANSDUCTION; TIME FACTOR;

ANIMALS; APOPTOSIS; BINDING SITES; CELLS, CULTURED; DISEASE MODELS, ANIMAL; INTERLEUKIN-17; MALE; MICE, INBRED C57BL; MYOCARDIAL INFARCTION; MYOCARDIAL REPERFUSION INJURY; MYOCYTES, CARDIAC; NITRIC OXIDE SYNTHASE TYPE II; PHOSPHORYLATION; PROMOTER REGIONS, GENETIC; RECEPTORS, INTERLEUKIN-17; SIGNAL TRANSDUCTION; STAT3 TRANSCRIPTION FACTOR; TIME FACTORS; TRANSFECTION; TYRPHOSTINS;

EID: 84985986745     PISSN: 01674889     EISSN: 18792596     Source Type: Journal    
DOI: 10.1016/j.bbamcr.2016.08.013     Document Type: Article

References (35)

1. [1] Orogo, A.M., Gustafsson, A.B., Cell death in the myocardium: my heart won't go on. IUBMB Life 65 (2013), 651–656.
2. [2] Isailovic, N., Daigo, K., Mantovani, A., Selmi, C., Interleukin-17A nd innate immunity in infections and chronic inflammation. J. Autoimmun. 60 (2015), 1–11.
3. [3] Baldeviano, G.C., Barin, J.G., Talor, M.V., Srinivasan, S., Bedja, D., Zheng, D., Gabrielson, K., Iwakura, Y., Rose, N.R., Cihakova, D., Interleukin-17A is dispensable for myocarditis but essential for the progression to dilated cardiomyopathy. Circ. Res. 106 (2010), 1646–1655.
4. [4] Zhou, S.F., Yuan, J., Liao, M.Y., Xia, N., Tang, T.T., Li, J.J., Jiao, J., Dong, W.Y., Nie, S.F., Zhu, Z.F., Zhang, W.C., Lv, B.J., Xiao, H., Wang, Q., Tu, X., Liao, Y.H., Shi, G.P., Cheng, X., IL-17A promotes ventricular remodeling after myocardial infarction. J. Mol. Med. 92 (2014), 1105–1116.
5. [5] Savvatis, K., Pappritz, K., Becher, P.M., Lindner, D., Zietsch, C., Volk, H.D., Westermann, D., Schultheiss, H.P., Tschope, C., Interleukin-23 deficiency leads to impaired wound healing and adverse prognosis after myocardial infarction. Circ. Heart Fail. 7 (2014), 161–171.
6. [6] Barry, S.P., Ounzain, S., McCormick, J., Scarabelli, T.M., Chen-Scarabelli, C., Saravolatz, L.I., Faggian, G., Mazzucco, A., Suzuki, H., Thiemermann, C., Knight, R.A., Latchman, D.S., Stephanou, A., Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury. Int. J. Cardiol. 163 (2013), 326–334.
7. [7] Siti, H.N., Kamisah, Y., Kamsiah, J., The role of oxidative stress, antioxidants and vascular inflammation in cardiovascular disease (a review). Vasc. Pharmacol. 71 (2015), 40–56.
8. [8] Jones, S.P., Bolli, R., The ubiquitous role of nitric oxide in cardioprotection. J. Mol. Cell. Cardiol. 40 (2006), 16–23.
9. [9] Hausenloy, D.J., Yellon, D.M., The second window of preconditioning (SWOP) where are we now?. Cardiovasc. Drugs Ther. 24 (2010), 235–254.
10. [10] Frustaci, A., Russo, M.A., Morgante, E., Scopelliti, F., Aquilano, K., Ciriolo, M.R., Grande, C., Verardo, R., Chimenti, C., Oxidative myocardial damage in human cocaine-related cardiomyopathy. Eur. J. Heart Fail. 17 (2015), 283–290.
11. [11] Razavi, H.M., Hamilton, J.A., Feng, Q., Modulation of apoptosis by nitric oxide: implications in myocardial ischemia and heart failure. Pharmacol. Ther. 106 (2005), 147–162.
12. [12] Yoon, J.H., Sudo, K., Kuroda, M., Kato, M., Lee, I.K., Han, J.S., Nakae, S., Imamura, T., Kim, J., Ju, J.H., Kim, D.K., Matsuzaki, K., Weinstein, M., Matsumoto, I., Sumida, T., Mamura, M., Phosphorylation status determines the opposing functions of Smad2/Smad3 as STAT3 cofactors in TH17 differentiation. Nat. Commun., 6, 2015, 7600.
13. [13] Hirahara, K., Ghoreschi, K., Laurence, A., Yang, X.P., Kanno, Y., O'Shea, J.J., Signal transduction pathways and transcriptional regulation in Th17 cell differentiation. Cytokine Growth Factor Rev. 21 (2010), 425–434.
14. [14] Lo, H.W., Hsu, S.C., Ali-Seyed, M., Gunduz, M., Xia, W., Wei, Y., Bartholomeusz, G., Shih, J.Y., Hung, M.C., Nuclear interaction of EGFR and STAT3 in the activation of the iNOS/NO pathway. Cancer Cell 7 (2005), 575–589.
15. [15] Yu, Z., Kone, B.C., The STAT3 DNA-binding domain mediates interaction with NF-kappaB p65 and inducible nitric oxide synthase transrepression in mesangial cells. J. Am. Soc. Nephrol. 15 (2004), 585–591.
16. [16] Yu, Z., Zhang, W., Kone, B.C., Signal transducers and activators of transcription 3 (STAT3) inhibits transcription of the inducible nitric oxide synthase gene by interacting with nuclear factor kappaB. Biochem. J. 367 (2002), 97–105.
17. [17] Chittezhath, M., Deep, G., Singh, R.P., Agarwal, C., Agarwal, R., Silibinin inhibits cytokine-induced signaling cascades and down-regulates inducible nitric oxide synthase in human lung carcinoma A549 cells. Mol. Cancer Ther. 7 (2008), 1817–1826.
18. [18] Smyth, J.W., Hong, T.T., Gao, D., Vogan, J.M., Jensen, B.C., Fong, T.S., Simpson, P.C., Stainier, D.Y., Chi, N.C., Shaw, R.M., Limited forward trafficking of connexin 43 reduces cell-cell coupling in stressed human and mouse myocardium. J. Clin. Invest. 120 (2010), 266–279.
19. [19] Hu, X., Zhang, L., Jin, J., Zhu, W., Xu, Y., Wu, Y., Wang, Y., Chen, H., Webster, K.A., Chen, H., Yu, H., Wang, J., Heparanase released from mesenchymal stem cells activates integrin beta1/HIF-2alpha/Flk-1 signaling and promotes endothelial cell migration and angiogenesis. Stem Cells 33 (2015), 1850–1862.
20. [20] 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., Yuan, J., Jevallee, H., Wei, F., Shi, G.P., Cheng, X., Interleukin-17A contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration. J. Am. Coll. Cardiol. 59 (2012), 420–429.
21. [21] Fang, Y., Sang, H., Yuan, N., Sun, H., Yao, S., Wang, J., Qin, S., Ethanolic extract of propolis inhibits atherosclerosis in ApoE-knockout mice. Lipids Health Dis., 12, 2013, 123.
22. [22] Wei, Z., Wang, Y., Zhang, K., Liao, Y., Ye, P., Wu, J., Wang, Y., Li, F., Yao, Y., Zhou, Y., Liu, J., Inhibiting the Th17/IL-17A-related inflammatory responses with digoxin confers protection against experimental abdominal aortic aneurysm. Arterioscler. Thromb. Vasc. Biol. 34 (2014), 2429–2438.
23. [23] Yan, X., Shichita, T., Katsumata, Y., Matsuhashi, T., Ito, H., Ito, K., Anzai, A., Endo, J., Tamura, Y., Kimura, K., Fujita, J., Shinmura, K., Shen, W., Yoshimura, A., Fukuda, K., Sano, M., Deleterious effect of the IL-23/IL-17A axis and gammadeltaT cells on left ventricular remodeling after myocardial infarction. J. Am. Heart Assoc., 1, 2012, e4408.
24. [24] 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., Neutrophils, neutrophil extracellular traps and interleukin-17A ssociate with the organisation of thrombi in acute myocardial infarction. Thromb. Haemost. 109 (2013), 290–297.
25. [25] Galluzzi, L., Vitale, I., Abrams, J.M., Alnemri, E.S., Baehrecke, E.H., Blagosklonny, M.V., Dawson, T.M., Dawson, V.L., El-Deiry, W.S., Fulda, S., Gottlieb, E., Green, D.R., Hengartner, M.O., Kepp, O., Knight, R.A., Kumar, S., Lipton, S.A., Lu, X., Madeo, F., Malorni, W., Mehlen, P., Nunez, G., Peter, M.E., Piacentini, M., Rubinsztein, D.C., Shi, Y., Simon, H.U., Vandenabeele, P., White, E., Yuan, J., Zhivotovsky, B., Melino, G., Kroemer, G., Molecular definitions of cell death subroutines: recommendations of the nomenclature committee on cell death 2012. Cell Death Differ. 19 (2012), 107–120.
26. [26] Maarsingh, H., Zaagsma, J., Meurs, H., Arginase: a key enzyme in the pathophysiology of allergic asthma opening novel therapeutic perspectives. Br. J. Pharmacol. 158 (2009), 652–664.
27. [27] Whyte, J.J., Laughlin, M.H., The effects of acute and chronic exercise on the vasculature. Acta Physiol (Oxf.) 199 (2010), 441–450.
28. [28] Miljkovic, D., Trajkovic, V., Inducible nitric oxide synthase activation by interleukin-17. Cytokine Growth Factor Rev. 15 (2004), 21–32.
29. [29] Godecke, A., Molojavyi, A., Heger, J., Flogel, U., Ding, Z., Jacoby, C., Schrader, J., Myoglobin protects the heart from inducible nitric-oxide synthase (iNOS)-mediated nitrosative stress. J. Biol. Chem. 278 (2003), 21761–21766.
30. [30] Reinartz, M., Ding, Z., Flogel, U., Godecke, A., Schrader, J., Nitrosative stress leads to protein glutathiolation, increased s-nitrosation, and up-regulation of peroxiredoxins in the heart. J. Biol. Chem. 283 (2008), 17440–17449.
31. [31] Chaturvedi, M.M., Sung, B., Yadav, V.R., Kannappan, R., Aggarwal, B.B., NF-kappaB addiction and its role in cancer: 'one size does not fit all'. Oncogene 30 (2011), 1615–1630.
32. [32] Haghikia, A., Ricke-Hoch, M., Stapel, B., Gorst, I., Hilfiker-Kleiner, D., STAT3, a key regulator of cell-to-cell communication in the heart. Cardiovasc. Res. 102 (2014), 281–289.
33. [33] Dawn, B., Xuan, Y.T., Guo, Y., Rezazadeh, A., Stein, A.B., Hunt, G., Wu, W.J., Tan, W., Bolli, R., IL-6 plays an obligatory role in late preconditioning via JAK-STAT signaling and upregulation of iNOS and COX-2. Cardiovasc. Res. 64 (2004), 61–71.
34. [34] Mattila, J.T., Thomas, A.C., Nitric oxide synthase: non-canonical expression patterns. Front. Immunol., 5, 2014, 478.
35. [35] Fahmi, A., Smart, N., Punn, A., Jabr, R., Marber, M., Heads, R., p42/p44-MAPK and PI3K are sufficient for IL-6 family cytokines/gp130 to signal to hypertrophy and survival in cardiomyocytes in the absence of JAK/STAT activation. Cell. Signal. 25 (2013), 898–909.