Document Detail

Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function.
MedLine Citation:
PMID:  25128167     Owner:  NLM     Status:  Publisher    
Regulatory T cells (Tregs) play a pivotal role in suppressing immune responses regulating behavior and gene expression in effector T cells, macrophages and dendritic cells. Tregs infiltrate the infarcted myocardium; however, their role the inflammatory and reparative response following myocardial infarction remains poorly understood. We used foxp3(EGFP) reporter mice to study Treg trafficking in the infarcted heart and we examined the effects of Treg depletion on post-infarction remodeling using an anti-CD25 antibody. Moreover, we investigated the in vitro effects of Tregs on cardiac fibroblast phenotype and function. Low numbers of Tregs infiltrated the infarcted myocardium after 24-72h of reperfusion. Treg depletion had no significant effects on cardiac dysfunction and scar size following reperfused myocardial infarction, but accelerated ventricular dilation and accentuated apical remodeling. Enhanced myocardial dilation in Treg-depleted animals was associated with increased expression of the CC chemokine CCL2 and accentuated macrophage infiltration. In vitro, Tregs modulated cardiac fibroblast phenotype, reducing expression of alpha-smooth muscle actin, decreasing expression of matrix metalloproteinase-3 and attenuating contraction of fibroblast-populated collagen pads. Our findings suggest that endogenous Tregs have modest effects on the inflammatory and reparative response following myocardial infarction. However, the anti-inflammatory and matrix-preserving properties of Tregs may suggest a role for Treg-based cell therapy in attenuation of adverse post-infarction remodeling.
Amit Saxena; Marcin Dobaczewski; Vikrant Rai; Zaffar Haque; Wei Chen; Na Li; Nikolaos G Frangogiannis
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-8-15
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  -     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2014 Aug 
Date Detail:
Created Date:  2014-8-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014, American Journal of Physiology - Heart and Circulatory Physiology.
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