Time-dependent changes in myocardial structure following discrete injury in mice deficient of matrix metalloproteinase-3

Mukherjee, Rupak; Bruce, James A.; McClister, David M.; Allen, Claire M.; Sweterlitsch, Sarah E.; Saul, J. Philip

doi:10.1016/j.yjmcc.2005.03.012

Cited by 25 publications

(22 citation statements)

References 46 publications

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“…The consequences of gene deletion of stromelysin MMP-3, or matrilysin MMP-7, have been examined in murine models of myocardial injury (238,284). In the MMP-3 null mice, abnormalities in the immune response have been demonstrated which included defects in cellular proliferation and cytokine release (479).…”

Section: A Targeted Gene Deletion Of Mmpsmentioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

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It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

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Section: A Targeted Gene Deletion Of Mmpsmentioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

1,005

1,023

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“…These MMPs are generated by a wide variety of cells such as fibroblasts, endothelial cells, osteoblasts, macrophages, lymphocytes, and neutrophils. Matrix metalloproteinase-3 (MMP-3), also termed stromelysin-1, has been reported to play a role in the organization of dermal wound healing [Bullard et al, 1999] and myocardial wound healing [Mukherjee et al, 2005], as well as the degradation of collagens (types III, IV, V, and IX), gelatin, aggrecan, versican, perlecan, decorin, proteoglycan, fibronectin, laminin, and osteonectin [Chakraborti et al, 2003]. In fact, MMP-3 degrades perlecan in human umbilical arterial endothelial-cell basement membranes to release basic fibroblast growth factor (bFGF) [Whitelock et al, 1996].…”

mentioning

confidence: 99%

MMP‐3 provokes CTGF/CCN2 production independently of protease activity and dependently on dynamin‐related endocytosis, which contributes to human dental pulp cell migration

Muromachi

Kamio

Narita

et al. 2012

J of Cellular Biochemistry

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Matrix metalloproteinase-3 (MMP-3) expression is promoted after pulpotomy, and application of MMP-3 to dental pulp after pulpotomy accelerates angiogenesis and hard tissue formation. However, the mechanism by which MMP-3 promotes dental pulp wound healing is still unclear. Connective tissue growth factor/CCN family 2 (CTGF/CCN2), a protein belonging to the CCN family, is considered to participate in wound healing, angiogenesis, and cell migration. In this study, we examined the involvement of CTGF/CCN2 in MMP-3-induced cell migration in human dental pulp (fibroblast-like) cells. In human dental pulp cells, MMP-3 promoted cell migration, but this effect was clearly blocked in the presence of anti-CTGF/CCN2 antibody. MMP-3 provoked mRNA and protein expression and secretion of CTGF/CCN2 in a concentration- and time-dependent manner. The MMP-3 inhibitor NNGH failed to suppress MMP-3-induced CTGF/CCN2 protein expression. The potent dynamin inhibitor dynasore clearly inhibited MMP-3-induced CTGF/CCN2 expression. These results strongly suggest that MMP-3 induces CTGF/CCN2 production independently of the protease activity of MMP-3 and dependently on dynamin-related endocytosis, which is involved in cell migration in human dental pulp cells.

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“…MMP2 is involved in macrophage tissue infiltration after myocardial infarction by generating chemoattractive fragments from ECM proteins [57]. MMP3 facilitates macrophage migration to the area of myocardial injury [74]. MMP13 has been shown to be involved in ECM proteolysis in a model of Matrigel basement membrane in vitro and in vivo [75].…”

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confidence: 99%

Extracellular proteolysis in macrophage migration: Losing grip for a breakthrough

et al. 2011

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Macrophage tissue infiltration is a hallmark of several pathological situations including cancer, neurodegenerative disorders and chronic inflammation. Hence, deciphering the mechanisms of macrophage migration across a variety of tissues holds great potential for novel anti-inflammatory therapies. Leukocytes have long been thought to migrate through tissues by using the amoeboid (protease-independent) migration mode; however, recent evidence indicates that macrophages can use either the amoeboid or the mesenchymal (protease-dependent) migration mode depending on the environmental constraints. Proteolytic activity is required for several key processes including cell migration. Paradoxically, the role of proteases in macrophage migration has been poorly studied. Here, by focusing on the best characterized extracellular protease families -MMPs, cathepsins and urokinase-type plasminogen activator -we give an overview of their probable involvement in macrophage migration. These proteases appear to play a role in all of the situations encountered by migrating macrophages, i.e. diapedesis, 2D and 3D migration. Migration of macrophages across tissues seems to proceed through an integrative analysis of numerous environmental clues allowing the cells to adapt their migration mode (amoeboid/ mesenchymal) and secrete dedicated proteases to ensure efficient tissue infiltration, as discussed in this review. The role of proteases in macrophage migration is an emerging field of research, which deserves further work to allow a more precise understanding.Key words: Cathepsins . Macrophage . MMPs . Migration . Proteases IntroductionTrafficking of leukocytes is a key process for immune cell development and host defense (reviewed in [1]); however, the presence of phagocyte-infiltrated tissues often correlates with the aggravation of several diseases including cancers, neurodegenerative disorders, atherosclerosis and chronic inflammation.Given this, the specific targeting of phagocyte tissue infiltration, without affecting the migration of the other leukocyte subsets required for protective immunity, is a challenge for the future. The identification of the migration modes and molecular processes used by macrophages to infiltrate tissues will therefore be key for proposing new therapeutic approaches.Phagocytes are able to migrate through most tissues in the body and, in vivo, they encounter both 2-dimentional (2D) and 3-dimentional (3D) environments. 2D migration takes place along surfaces such as inner vessel walls and inner epithelial surfaces (peritoneal cavity or lung alveolae) and involves firm cell adhesion Mini-Review to the substratum. 3D migration takes place inside tissues composed of cells and extracellular matrix (ECM) components which constitute a complex and heterogeneous environment. It has been observed that for tumor cells 2D and 3D migration proceed through distinct molecular and cellular mechanisms [2,3]. Phagocyte migration in 2D and across endothelial surfaces has been studied using a large panel of in vitro model...

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Time-dependent changes in myocardial structure following discrete injury in mice deficient of matrix metalloproteinase-3

Cited by 25 publications

References 46 publications

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

MMP‐3 provokes CTGF/CCN2 production independently of protease activity and dependently on dynamin‐related endocytosis, which contributes to human dental pulp cell migration

Extracellular proteolysis in macrophage migration: Losing grip for a breakthrough

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