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Han Y, Liao X, Gao Z, et al. Cardiac troponin I exacerbates myocardial ischaemia/reperfusion injury by inducing the adhesion of monocytes to vascular endothelial cells via a TLR4/NF-κB-dependent pathway. Clin Sci (Lond). 2016;130(24):2279-2293doi: 10.1042/CS20160373.
Han, Y., Liao, X., Gao, Z., Yang, S., Chen, C., Liu, Y., Wang, W. E., Wu, G., Chen, X., Jose, P. A., Zhang, Y., & Zeng, C. (2016). Cardiac troponin I exacerbates myocardial ischaemia/reperfusion injury by inducing the adhesion of monocytes to vascular endothelial cells via a TLR4/NF-κB-dependent pathway. Clinical science (London, England : 1979), 130(24), 2279-2293. https://doi.org/10.1042/CS20160373
Han, Yu, et al. "Cardiac troponin I exacerbates myocardial ischaemia/reperfusion injury by inducing the adhesion of monocytes to vascular endothelial cells via a TLR4/NF-κB-dependent pathway." Clinical science (London, England : 1979) vol. 130,24 (2016): 2279-2293. doi: https://doi.org/10.1042/CS20160373
Han Y, Liao X, Gao Z, Yang S, Chen C, Liu Y, Wang WE, Wu G, Chen X, Jose PA, Zhang Y, Zeng C. Cardiac troponin I exacerbates myocardial ischaemia/reperfusion injury by inducing the adhesion of monocytes to vascular endothelial cells via a TLR4/NF-κB-dependent pathway. Clin Sci (Lond). 2016 Dec 01;130(24):2279-2293. doi: 10.1042/CS20160373. Epub 2016 Sep 28. PMID: 27682003.
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Clin Sci (Lond). 2016 Dec 01;130(24):2279-2293. doi: 10.1042/CS20160373. Epub 2016 Sep 28.

Cardiac troponin I exacerbates myocardial ischaemia/reperfusion injury by inducing the adhesion of monocytes to vascular endothelial cells via a TLR4/NF-κB-dependent pathway.

Clinical science (London, England : 1979)

Yu Han, Xiang Liao, Zhao Gao, Sufei Yang, Caiyu Chen, Yukai Liu, Wei Eric Wang, Gengze Wu, Xiongwen Chen, Pedro A Jose, Ye Zhang, Chunyu Zeng

Affiliations

  1. Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, 400042, P.R. China.
  2. Chongqing Institute of Cardiology, Chongqing Key Laboratory for Hypertension Research, Chongqing, 400042, P.R. China.
  3. Cardiovascular Research Center & Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
  4. Department of Medicine, Division of Renal Disease and Hypertension, The George Washington University School of Medicine & Health Sciences, Washington D.C., 20037, U.S.A.
  5. Department of Pharmacology and Physiology, The George Washington University School of Medicine & Health Sciences, Washington D.C., 20037, U.S.A.
  6. Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, 400042, P.R. China [email protected]) [email protected].

PMID: 27682003 DOI: 10.1042/CS20160373

Abstract

Cardiac troponin I (cTnI), a biomarker for myocardial damage and risk stratification, may be involved in the pathogenesis of cardiovascular diseases, which was ascribed to the effect of cTnI auto-antibodies. Whether or not cTnI itself has a direct impact on acute myocardial injury is unknown. To exclude the influence of cTnI antibody on the cardiac infarct size, we studied the effect of cTnI shortly after myocardial ischaemia-reperfusion (I/R) injury when cTnI antibodies were not elevated. Pretreatment with cTnI augmented the myocardial infarct size caused by I/R, accompanied by an increase in inflammatory markers in the blood and myocardium. Additional experiments using human umbilical vein endothelial cells (HUVECs) showed that the detrimental effect of cTnI was related to cTnI-induced increase in vascular cell adhesion molecule-1 (VCAM-1) expression and VCAM-1 mediated adhesion of human monocytes (THP-1) to HUVECs, which could be neutralized by VCAM-1 antibody. Both toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) were involved in the signalling pathway, because blockade of either TLR4 or NF-κB inhibited the cTnI's effect on VCAM-1 expression and adhesion of monocytes to endothelial cells. Moreover, TLR4 inhibition reduced cTnI-augmented cardiac injury in rats with I/R injury. We conclude that cTnI exacerbates myocardial I/R injury by inducing the adhesion of monocytes to vascular endothelial cells via activation of the TLR4/NF-κB pathway. Inhibition of TLR4 may be an alternative strategy to reduce cTnI-induced myocardial I/R injury.

© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society.

Keywords: adhesion factor; cardiac troponin I; coronary heart disease; endothelial cell; myocardial ischaemia–reperfusion injury

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