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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Heart+Circ+Physiol
2014 ; 307
(8
): H1233-42
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Regulatory T cells are recruited in the infarcted mouse myocardium and may
modulate fibroblast phenotype and function
#MMPMID25128167
Saxena A
; Dobaczewski M
; Rai V
; Haque Z
; Chen W
; Li N
; Frangogiannis NG
Am J Physiol Heart Circ Physiol
2014[Oct]; 307
(8
): H1233-42
PMID25128167
show ga
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 after myocardial infarction remains
poorly understood. We used FoxP3(EGFP) reporter mice to study Treg trafficking in
the infarcted heart and examined the effects of Treg depletion on postinfarction
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 24-72 h of reperfusion. Treg
depletion had no significant effects on cardiac dysfunction and scar size after
reperfused myocardial infarction but accelerated ventricular dilation and
accentuated apical remodeling. Enhanced myocardial dilation in Treg-depleted
animals was associated with increased expression of chemokine (C-C motif) ligand
2 and accentuated macrophage infiltration. In vitro, Tregs modulated the cardiac
fibroblast phenotype, reducing expression of ?-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 after myocardial
infarction. However, the anti-inflammatory and matrix-preserving properties of
Tregs may suggest a role for Treg-based cell therapy in the attenuation of
adverse postinfarction remodeling.