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Transcript 
Matrix Metalloproteinase-28 Deletion Exacerbates Cardiac
Dysfunction and Rupture After Myocardial Infarction in
Mice by Inhibiting M2 Macrophage ActivationNovelty and
Significance
by Yonggang Ma, Ganesh V. Halade, Jianhua Zhang, Trevi A. Ramirez, Daniel Levin,
Andrew Voorhees, Yu-Fang Jin, Hai-Chao Han, Anne M. Manicone, and Merry L.
Lindsey
Circulation Research
Volume 112(4):675-688
February 15, 2013
Copyright © American Heart Association, Inc. All rights reserved.
Expression patterns and cellular source of matrix metalloproteinase (MMP)-28 at baseline and
post–myocardial infarction (MI).
Yonggang Ma et al. Circ Res. 2013;112:675-688
Copyright © American Heart Association, Inc. All rights reserved.
Matrix metalloproteinase-28 (MMP) deletion decreased survival, increased cardiac rupture, and
exacerbated left ventricle (LV) dysfunction post–myocardial infarction.
Yonggang Ma et al. Circ Res. 2013;112:675-688
Copyright © American Heart Association, Inc. All rights reserved.
M2 macrophage activation was impaired with matrix metalloproteinase (MMP)-28 deletion.
Yonggang Ma et al. Circ Res. 2013;112:675-688
Copyright © American Heart Association, Inc. All rights reserved.
Matrix metalloproteinase (MMP)-28 deletion attenuated macrophages polarization toward M2
subtype.
Yonggang Ma et al. Circ Res. 2013;112:675-688
Copyright © American Heart Association, Inc. All rights reserved.
Collagen deposition, lysyl oxidase content, and collagen cross-linking were reduced with matrix
metalloproteinase (MMP)-28 deletion.
Yonggang Ma et al. Circ Res. 2013;112:675-688
Copyright © American Heart Association, Inc. All rights reserved.
Matrix metalloproteinase (MMP-28) deletion reduced myofibroblast numbers at day 7 post–
myocardial infarction (MI) and affected myofibroblast function.
Yonggang Ma et al. Circ Res. 2013;112:675-688
Copyright © American Heart Association, Inc. All rights reserved.
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