Furin and membrane type‐1 metalloproteinase mRNA levels and activation of metalloproteinase‐2 are associated with arterial remodeling

Kleijn, Dominique P.V. de; Sluijter, Joost P.G.; Smit, J. M.; Velema, Evelyn; Richard, Wietske; Schoneveld, Arjan H.; Pasterkamp, Gérard; Borst, Cornelius

doi:10.1016/s0014-5793(01)02622-9

Cited by 41 publications

(35 citation statements)

References 26 publications

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“…have shown that proMT1-MMP has to be processed to activate MMP2 (Pei and Weiss, 1996;Yu et al, 1997;Cao et al, 1998;Yana and Weiss, 2000). Recently, several laboratories have generated a wealth of data showing strong correlations between furin activity and those of MT1-MMP and MMP2 (Maquoi et al, 1998;Bassi et al, 2001;de Kleijn et al, 2001). Moreover, several groups have found proMT1-MMP at the plasma membrane of different cell lines, adding weight to the proposition that the pro-domain of MT1-MMP is required for the efficient trafficking of the enzyme to the cell surface (Sato et al, 1994;Sternlicht and Werb, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Although it has been demonstrated that full-length proMT1-MMP is the prominent form appearing at the plasma membrane of many cell types, the subcellular site of activation and the identity of the activating enzyme remain controversial (Sato et al, 1994;Okumura et al, 1997;Cao et al, 1998;Lehti et al, 1998;Sternlicht and Werb, 2001). Nonetheless, a proprotein-convertase/MT1-MMP/MMP2 axis has been proposed to conduct ECM remodeling (Yana and Weiss, 2000;de Kleijn et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Furin interacts with proMT1-MMP and integrin αV at specialized domains of renal cell plasma membrane

Mayer

Boileau

Bendayan

2003

Journal of Cell Science

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Matrix metalloproteinases (MMPs) and integrins are essential for cell and extracellular matrix homeostasis. Both membrane type-1 MMP (MT1-MMP) and the integrin αV subunit are fully activated upon cleavage at a furin recognition site. Furin is shuttled to the cell surface through the trans-Golgi network and endosomal system, and its only known role on plasma membrane consists in activation of opportunistic pathogenic entities. Here, we report findings about the interaction of furin with MT1-MMP and the integrinαV at the cell surface. By using in vivo gene delivery, western blotting and immunogold electron microscopy, we provide evidence of significant pools of furin and proMT1-MMP along the surface of cells lining basement membranes. Moreover, furin and integrin αV are frequently found associated with the slit diaphragm of renal podocytes and around endothelial fenestrations. ProMT1-MMP, by contrast, is concentrated at the slit diaphragm. Coimmunoprecipitations and double immunogold labelings indicate that furin interacts with proMT1-MMP and αV at points of insertion of the slit diaphragm. Our results suggest that these focalized complexes could trigger basement membrane proteolysis either directly by activation of proMT1-MMP or indirectly by promoting activation of proMMP2.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Furin interacts with proMT1-MMP and integrin αV at specialized domains of renal cell plasma membrane

Mayer

Boileau

Bendayan

2003

Journal of Cell Science

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“…47 It is still unclear how the vascular wall senses these biomechanical effects, but the endothelium plays an important role in its response. 1 Flow changes can upregulate activation of MMPs, 48 which are considered to be important for remodeling in general. 49,50,26 Endothelial cells sense shear stress and various patterns of flow by regulating the expression of intracellular adhesion molecule 1, vascular adhesion molecule 1, 51 monocyte chemoattractant molecule 1, 52 and MMP-9.…”

Section: Expansive Remodeling: a Role For Innate Immunity?mentioning

confidence: 99%

Expansive Arterial Remodeling: Location, Location, Location

Pasterkamp

Galis

Kleijn

2004

ATVB

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118

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Abstract-The artery is a dynamic organ capable of changing its geometry in response to atherosclerotic plaque formation.Expansion of the vessel diameter retards luminal narrowing and is considered a compensatory response. However, the expansive remodeling response is a "wolf in sheep's clothes," because expansion is associated with the presence of inflammatory cells, proteolysis, and a thrombotic plaque phenotype. The prevalence and clinical presentation of expansively remodeled lesions may differ among vascular beds. However, it is evident that all types of atherosclerotic arterial expansive lesions share the presence of inflammatory cells and subsequent protease activities. The potential role of inflammation and protease activity in the development of the different remodeling modes is discussed. Key Words: remodeling Ⅲ atherosclerosis Ⅲ toll-like receptor Ⅲ inflammation Ⅲ compensatory enlargement P laque formation has long been considered the only determinant of atherosclerotic luminal narrowing. The arterial wall, however, is not a rigid tube, but rather an organ capable of overall reshaping in response to hemodynamic, mechanical, and biochemical stimuli. For instance, the increase in the circumference of the artery can partially or totally compensate for the encroachment of the lumen caused by formation of atherosclerotic plaques or by intimal hyperplasia after arterial injury. 1-3 However, the arterial wall may also respond with constrictive remodeling, thereby aggravating the luminal narrowing response 4,5 (Figure 1).Scientific interest in the role of arterial remodeling in occlusive arterial disease boomed with the upcoming use of the visualization technique of intravascular ultrasound (IVUS). With IVUS, it became apparent just how ubiquitously remodeling can prevent plaque from encroaching on the lumen and also how failure of an expansive remodeling response accelerates luminal stenosis in de novo atherosclerosis. The role of such geometrical remodeling response in relation to plaque formation is currently appreciated but has been traditionally strongly underestimated as a causal factor for arterial occlusive disease. It has recently become clear that the geometrical change in arterial size and plaque area may equally contribute to the luminal narrowing in atherosclerotic disease 6 (Figure 2). For instance, it is possible to demonstrate that in 5% of patients eligible for coronary intervention, the plaque mass at the culprit lesion is actually smaller than that located at the angiographically normal reference site, indicating that in such lesions the degree of luminal narrowing is determined by the differences in vessel size rather than by the plaque mass. 6 In this brief review, an overview of anatomical localization and local morphology of the different remodeling modes is given. We also discuss available results of mechanistic

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“…Matrix turnover in arteries occurs during arterial remodeling in response to sustained blood flow changes, 11,12 balloon injury, 13,14 and atherosclerotic plaque formation. 15 Arterial remodeling, which can be outward to reduce lumen loss and inward to increase lumen loss, is characterized by structural changes of the arterial wall involving cell migration and collagen (matrix) breakdown 16 by matrix metalloproteases (MMPs), including MMP9, which can be stimulated by Tlr4 activation.…”

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confidence: 99%

Toll-Like Receptor 4 Is Involved in Outward Arterial Remodeling

et al. 2004

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Background-Toll-like receptor 4 (Tlr4) is the receptor for exogenous lipopolysaccharides (LPS). Expression of endogenous Tlr4 ligands, heat shock protein 60 (Hsp60) and extra domain A of fibronectin, has been observed in arthritic and oncological specimens in which matrix turnover is an important feature. In atherosclerosis, outward remodeling is characterized by matrix turnover and a structural change in arterial circumference and is associated with a vulnerable plaque phenotype. Since Tlr4 ligands are expressed during matrix turnover, we hypothesized that Tlr4 is involved in arterial remodeling. Methods and Results-In a femoral artery cuff model in the atherosclerotic ApoE3 (Leiden) transgenic mouse, Tlr4 activation by LPS stimulated plaque formation and subsequent outward arterial remodeling. With the use of the same model in wild-type mice, neointima formation and outward remodeling occurred. In Tlr4-deficient mice, however, no outward arterial remodeling was observed independent of neointima formation. Carotid artery ligation in wild-type mice resulted in outward remodeling without neointima formation in the contralateral artery. This was associated with an increase in Tlr4 expression and EDA and Hsp60 mRNA levels. In contrast, outward remodeling was not observed after carotid ligation in Tlr4-deficient mice. Conclusions-These findings provide genetic evidence that Tlr4 is involved in outward arterial remodeling, probably through upregulation of Tlr4 and Tlr4 ligands.

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Furin and membrane type‐1 metalloproteinase mRNA levels and activation of metalloproteinase‐2 are associated with arterial remodeling

Cited by 41 publications

References 26 publications

Furin interacts with proMT1-MMP and integrin αV at specialized domains of renal cell plasma membrane

Furin interacts with proMT1-MMP and integrin αV at specialized domains of renal cell plasma membrane

Expansive Arterial Remodeling: Location, Location, Location

Toll-Like Receptor 4 Is Involved in Outward Arterial Remodeling

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