Myocardial infarction causes inflammation and leukocyte recruitment at remote sites in the myocardium and in the renal g
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Inflammation Research
ORIGINAL RESEARCH PAPER
Myocardial infarction causes inflammation and leukocyte recruitment at remote sites in the myocardium and in the renal glomerulus Neil Ruparelia • Janet E. Digby • Andrew Jefferson • Debra J. Medway • Stefan Neubauer • Craig A. Lygate Robin P. Choudhury
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Received: 7 August 2012 / Revised: 11 January 2013 / Accepted: 12 February 2013 / Published online: 8 March 2013 Ó The Author(s) 2013. This article is published with open access at Springerlink.com
Abstract Rationale and Objective Acute myocardial infarction (AMI) results in the recruitment of leukocytes to injured myocardium. Additionally, myocardium remote to the infarct zone also becomes inflamed and is associated with adverse left ventricular remodelling. Renal ischaemic syndromes have been associated with remote organ inflammation and impaired function. Here, we tested the hypothesis that AMI results in remote organ (renal) inflammation. Methods Mice were subjected to either AMI, sham procedure or no procedure and the inflammatory response in peripheral blood, injured and remote myocardium, and kidneys was studied at 24 h. Results AMI resulted in increased circulating neutrophils (P \ 0.001) and monocytes (P \ 0.001). mRNA for inflammatory mediators significantly increased in infarcted myocardium and in remote myocardium. VCAM-1 mRNA was increased in both infarcted and remote myocardium. VCAM-1 protein was also increased in the kidneys of AMI Responsible Editor: Graham Wallace
Electronic supplementary material The online version of this article (doi:10.1007/s00011-013-0605-4) contains supplementary material, which is available to authorized users. N. Ruparelia J. E. Digby A. Jefferson S. Neubauer R. P. Choudhury (&) Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Headley Way, Oxford OX3 9DU, UK e-mail: [email protected] D. J. Medway C. A. Lygate Division of Cardiovascular Medicine, Radcliffe Department of Medicine, The Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK
mice (P \ 0.05) and immunofluorescence revealed localisation of VCAM-1 to glomeruli, associated with leukocyte infiltration and increased local inflammatory mRNA expression. Conclusions We conclude that in addition to local inflammation, AMI results in remote organ inflammation evidenced by (1) increased expression of mRNA for inflammatory cytokines, (2) marked upregulation of VCAM-1 in renal glomeruli, and (3) the recruitment and infiltration of leukocytes in the kidney. Keywords Inflammation Myocardial infarction Leukocytes Remote sites Renal glomerulus
Introduction Acute myocardial infarction (AMI) results in the activation of the acute phase response [1, 2] and mobilisation and recruitment of leukocytes to the site of infarcted myocardium [3, 4]. Furthermore, myocardium that is remote from ischaemic zones has also been associated with the activation of pro-inflammatory pathways and infiltra
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