The extracellular matrix as a modulator of the inflammatory and reparative response following myocardial infarction

被引:397
作者
Dobaczewski, Marcin [1 ]
Gonzalez-Quesada, Carlos [1 ]
Frangogiannis, Nikolaos G. [1 ]
机构
[1] Baylor Coll Med, Cardiovasc Sci Sect, Houston, TX 77030 USA
关键词
Myocardial infarction; Remodeling; Matrix Metalloproteinases; Hyaluronan; Collagen; Matricellular proteins; Myofibroblast; Cytokine; Chemokines; TGF-beta; Wound healing; MICE LACKING OSTEOPONTIN; METALLOPROTEINASE ACTIVITY; COLLAGEN DEGRADATION; CARDIAC DYSFUNCTION; REPERFUSION INJURY; ANGIOTENSIN-II; TISSUE-REPAIR; RAT-HEART; EXPRESSION; TENASCIN;
D O I
10.1016/j.yjmcc.2009.07.015
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The dynamic alterations in the cardiac extracellular matrix following myocardial infarction not only determine the mechanical properties of the infarcted heart, but also directly modulate the inflammatory and reparative response. During the inflammatory phase of healing, rapid activation of Matrix Metalloprotemases (MMP) causes degradation of the cardiac extracellular matrix. Matrix fragments exert potent proinflammatory actions, while MMPs process cytokines and chemokines altering their biological activity. In addition, vascular hyperpermeability results in extravasation of fibronectin and fibrinogen leading to formation of a plasma-derived provisional matrix that serves as a scaffold for leukocyte infiltration. Clearance of the infarct from dead cells and matrix debris is essential for resolution of inflammation and marks the transition to the proliferative phase. The fibrin-based provisional matrix is lysed and cellular fibronectin is secreted. ED-A fibronectin, mechanical tension and Transforming Growth Factor (TGF)-beta are essential for modulation of fibroblasts into mycifibroblasts, the main collagen-secreting cells in the wound. The matricellular proteins thrombospondin-1 and -2, osteopontin, tenascin-C, periostin, and secreted protein acidic and rich in cysteine (SPARC) are induced in the infarct regulating cellular interactions and promoting matrix organization. As the infarct matures, matrix cross-linking results in formation of a dense collagen-based scar. At this stage, shielding of fibroblasts from external mechanical tension by the mature matrix network may promote deactivation and cellular quiescence. The components of the extracellular matrix do not passively follow the pathologic alterations of the infarcted heart but critically modulate inflammatory and reparative pathways by transducing signals that affect cell survival, phenotype and gene expression. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:504 / 511
页数:8
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