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Role of expression IL-23 pathway in myocardial injury after global ischemia and reperfusion/cross talk with IL-17

American Journal of BioMedicine  Volume 2, Issue 8, pages1010– 1024 September 2014


Ling Ogiku; Runqiu Fujii; Song Xiao; Liu Xuehao

Abstract

Myocardial injury caused by global ischemia/reperfusion is a complicated pathophysiological course, in which inflammation is thought to play an important role. Endothelial dysfunction plays a critical role in the pathogenesis of reperfusion injury in the myocardium. This role stems from the close proximity of the endothelium to neutrophils and other inflammatory cell types at the vascular interface during the critical early phase as well as the later phase of reperfusion. IL-17A is a cytokine expressed by a variety of cells in response to inflammatory cytokines that are released following tissue injury and/or inflammation. IL-17A induces epithelial cells to secrete neutrophil chemoattractants. The cytokine IL-23, which can be produced by epithelial cells, plays an important role in IL-17A production. Global myocardial injury induced by abdominal heart transplant model in IL-17A deficient (Il17a-/-), IL-23R deficient (Il23r-/-) and WT mice. Our data showed that cTn-I, neutrophil accumulation MCP-1 and ICAM-1 were significantly less in both Il17a-/- mice and Il23r/- mice than in WT controls. These two pathways may become possible therapeutic targets for the treatment of global ischemia induced myocardial injury.

Keywords: Myocardial injury; Global ischemia/reperfusion; IL-17A; IL-23


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References

1. Jordan JE, Zhao ZQ, Vinten-Johansen J. The role of neutrophils in myocardial ischemia–reperfusion injury. Cardiovasc Res 1999; 43: 860–878. [PubMed]

2. Weisensee D, Bereiter-Hahn J, Schoeppe W, Low-Friedrich I. Effects of cytokines on the contractility of cultured cardiac myocytes. Int J Immunopharmacol 1993; 15:581-587. [PubMed]

3. Austin EW, Yousif NG, Ao L, Cleveland JC, Fullerton DA, Meng X. Ghrelin reduces myocardial injury following global ischemia and reperfusion via suppression of myocardial inflammatory response. American Journal of BioMedicine 2013;2(1): 38-48. [Abstract/Full Text]

4. Ferretti, S., Bonneau, O., Dubois, G.R., et al. IL-17, produced by lymphocytes and neutrophils, is necessary for lipopolysaccharide-induced airway neutrophilia: IL-15 as a possible trigger.
J. Immunol 2003;170: 2106–2112.
[PubMed]

5. Zelante T, De Luca A, Bonifazi P, Montagnoli C, Bozza S, et al. IL-23 and the Th17 pathway promote inflammation and impair antifungal immune resistance. Eur J Immunol 2007; 37: 2695–2706. [PubMed]

6. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. Establishment of a novel abdominal heart transplantation model of mice.2013; (5):1108-11. Chinese. [PubMed]

7. Su S, Türk TR, Wu S, Fan H, Fu J, Wu K, et. al. Modified suture technique in a mouse heart transplant model. Asian J Surg 2011;34(2):86-91. [PubMed]

8. Liu F, Kang SM. Heterotopic heart transplantation in mice. J Vis Exp 2007;(6):238. [PubMed]

9. Trinchieri G, Pflanz S, Kastelein RA. The IL-12 family of heterodimeric cytokines: New players in the regulation of T cell responses. Immunity 2003;19: 641–644. [PubMed]

10. Veldhoen M, Hocking RJ, Atkins CJ, Locksley RM, Stockinger B. TGF-β in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity 2006: 24: 179–189. [PubMed]

11. Linden A, Laan M, Anderson GP. Neutrophils, interleukin-17A and lung disease. Eur. Respir. J. 2005; 25: 159–172. [PubMed]

12. Alhasani S, Yousif NG. Critical role of IL-23 signaling in prostatic cancer.  American Journal of BioMedicine 2013; 1(1):4-6. [Abstract/Full Text]

13. Granado M, Fernandez N, Monge L, Figueras JC, Carreno-Tarragona G, Amor S, Garcia-Villalon AL. Effects of coronary ischemia-reperfusion in a rat model of early overnutrition: role of angiotensin receptors. PLoS One 2013; 8:e54984. [Abstract/Full Text]

14. Linden A, Laan M, Anderson GP. Neutrophils, interleukin-17A and lung disease. Eur. Respir. J. 2005; 25: 159–172. [PubMed]

15. Alidoosti M, Salarifar M, Zeinali AM, Kassaian SE, Dehkordi MR. Comparison of outcomes of percutaneous coronary intervention on proximal versus non-proximal left anterior descending coronary artery, proximal left circumflex, and proximal right coronary artery: a cross-sectional study. BMC Cardiovasc Disord 2007; 7:7. [PubMed]

16. Goudeau JJ, Clermont G, Guillery O, Lemaire-Ewing S, Musat A, Vernet M, et al. In high-risk patients, combination of anti-inflammatory procedures during cardiopulmonary bypass can reduce incidences of inflammation and oxidative stress. J Cardiovasc Pharmacol 2007; 49: 39–45. [PubMed]

17. Yousif NG, Al-Amran FG. Novel Toll-like receptor-4 deficiency attenuates trastuzumab (Herceptin) induced cardiac injury in mice. BMC Cardiovasc Disord 2011;11:62. [PubMed]

18. Wan S, DeSmet JM, Barvais L, Golstein M, Vincent JL, LeClerc JL. Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996; 112: 806–811. [PubMed]

19. Verma S, Fedak PW, Weisel RD, Szmitko PE, Badiwala MV, Bonneau D, et al. Off-pump coronary artery bypass surgery: fundamentals for the clinical cardiologist. Circulation 2004; 109: 1206–1211. [PubMed]

20. Slimani H, Zhai Y, Yousif NG, Ao L, Zeng Q, Fullerton DA, Meng X. Enhanced monocyte chemoattractant protein-1 production in aging mice exaggerates cardiac depression during endotoxemia. Crit Care 2014;18(5):527. [PubMed]

21. Prabhu SD. Cytokine-induced modulation of cardiac function. Circ Res 2004; 95:1140-1153. [PubMed]

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