The dynamic extracellular matrix: intervention strategies during heart failure and atherosclerosis

Heeneman, Sylvia; Cleutjens, J. P. M.; Faber, Birgit; Creemers, Esther E.; Suylen, Robert-Jan van; Lutgens, Esther; Cleutjens, Kitty B.J.M.; Daemen, Mat J.A.P.

doi:10.1002/path.1395

Cited by 120 publications

(115 citation statements)

References 104 publications

(98 reference statements)

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“…Therefore, STS can depress the Ang II-induced collagen type I expression through attenuating collagen synthesis. Moreover, it is known that collagen type I accumulation in the heart depends not only on its production, but also on its degradation, which is performed by proteinases, such as matrix metalloproteinase-1 (MMP-1) (Brilla et al, 1994;D'Armiento et al, 2002;Heeneman et al, 2003). As it is shown in Figure 4, Ang II significantly depressed MMP-1 expression and activity, which accorded with the previous reports (Chen et al, 2004a, b;Lijnen et al, 2006;Pan et al, 2008).…”

Section: Discussionsupporting

confidence: 89%

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Sodium tanshinone IIA sulfonate attenuates angiotensin II-induced collagen type I expression in cardiac fibroblasts in vitro

et al. 2009

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Cardiac fibrosis occurs after pathological stimuli to the cardiovascular system. One of the most important factors that contribute to cardiac fibrosis is angiotensin II (Ang II). Accumulating studies have suggested that reactive oxygen species (ROS) plays an important role in cardiac fibrosis and sodium tanshinone IIA sulfonate (STS) possesses antioxidant action. We therefore examined whether STS depresses Ang II-induced collagen type I expression in cardiac fibroblasts. In this study, Ang II significantly enhanced collagen type I expression and collagen synthesis. Meanwhile, Ang II depressed matrix metalloproteinase-1 (MMP-1) expression and activity. These responses were attenuated by STS. Furthermore, STS depressed the intracellular generation of ROS, NADPH oxidase activity and subunit p47 phox expression. In addition, N-acetylcysteine the ROS scavenger, depressed effects of Ang II in a manner similar to STS. In conclusion, the current studies demonstrate that anti-fibrotic effects of STS are mediated by interfering with the modulation of ROS.

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Section: Discussionsupporting

confidence: 89%

“…Cardiac fibroblasts (CFs) are the major source of collagen in the myocardium. Collagen type I accumulation in the heart depends not only on its production, but also on its degradation, which is performed by proteinases, such as matrix metalloproteinase-1 (MMP-1) (Heeneman et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Sodium tanshinone IIA sulfonate attenuates angiotensin II-induced collagen type I expression in cardiac fibroblasts in vitro

et al. 2009

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“…Section 1734 solely to indicate this fact. 1 Both authors contributed equally to this work. 2 To whom correspondence should be addressed: UAMS, Little Rock, AR…”

Section: Methodsmentioning

confidence: 99%

“…Among the extracellular matrix proteins, up to 85% are collagens, of which type 1 (collagen I) and type 3 (collagen III) constitute two-thirds of total collagens in most tissues (1). Transforming growth factor (TGF) 3 ␤ 1 is one of the most pleiotropic and multifunctional peptides known (2).…”

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confidence: 99%

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Regulation of TGFβ1-mediated Collagen Formation by LOX-1

Dandapat

Sun

et al. 2008

Journal of Biological Chemistry

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Transforming growth factor ␤ 1 (TGF␤ 1 ) activation leads to tissue fibrosis. Here, we report on the role of LOX-1, a lectin-like 52-kDa receptor for oxidized low density lipoprotein, in TGF␤ 1 -mediated collagen expression and underlying signaling in mouse cardiac fibroblasts. TGF␤ 1 was overexpressed in wildtype (WT) and LOX-1 knock-out mouse cardiac fibroblasts by transfection with adeno-associated virus type 2 vector carrying the active TGF␤ 1 moiety (AAV/TGF␤ 1 ACT ). Transfection of WT mouse cardiac fibroblasts with AAV/TGF␤ 1 ACT markedly enhanced the expression of NADPH oxidases (p22 phox , p47 phox , and gp91 phox subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases (MAPK). The TGF␤ 1 -mediated increase in collagen synthesis was markedly attenuated in the LOX-1 knock-out mouse cardiac fibroblasts as well as in WT mouse cardiac fibroblasts treated with a specific anti-LOX-1 antibody. Treatment with anti-LOX-1 antibody also reduced NADPH oxidase expression and MAPK activation. The NADPH oxidase inhibitors and gp91phox small interfering RNA reduced LOX-1 expression, MAPK activation, and collagen formation. The p38 MAPK inhibitors as well as the p44/42 MAPK inhibitors reduced collagen formation without affecting LOX-1 expression in cardiac fibroblasts. These observations suggest that collagen synthesis in cardiac fibroblasts involves a facilitative interaction between TGF␤ 1 -NADPH oxidase and LOX-1. Further, the activation of MAPK pathway appears to be downstream of TGF␤ 1 -reactive oxygen species-LOX-1 cascade.Cardiac fibrosis, characterized by accumulation of matrix proteins in the extracellular space in the perivascular region, is closely associated with the development of heart failure. Among the extracellular matrix proteins, up to 85% are collagens, of which type 1 (collagen I) and type 3 (collagen III) constitute two-thirds of total collagens in most tissues (1). Transforming growth factor (TGF) 3 ␤ 1 is one of the most pleiotropic and multifunctional peptides known (2). It exerts potent effects on many different cell types and is involved in a wide variety of biological processes (2). The cellular actions of TGF␤ 1 are dependent not only on the cell type but also on its state of differentiation and the cytokine milieu (3). Although there is evidence that TGF␤ 1 stimulates fibroblast growth, enhances collagen synthesis, and suppresses collagen degradation (2) ACT that appears to be functionally relevant in the process of ischemia-reperfusion (5).LOX-1 is a lectin-like receptor for oxidized low density lipoprotein (6). It is also up-regulated in response to oxidative stress (7). Activation of LOX-1 enhances the growth of cardiac fibroblasts and promotes collagen synthesis (8, 9). It has been reported that TGF␤ 1 can regulate LOX-1 expression in vascular endothelial cells, smooth muscle cells, and monocytes/macrophages (10, 11). Another study showed that LOX-1 blockade reduc...

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MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis

Hua

Dong

Zhang

et al. 2016

The Anatomical Record

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The miRNAs play important roles in regulating myocardial fibrosis. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in cardiac fibrosis in vitro and in vivo. In vitro experiment, Ang II-induced cardiac fibroblasts (CFBs) are transfected with pre-miR-214, anti-miR-214 and their oligo controls. Gene expression was checked by Quantitative realtime-PCR (qRT-PCR) and western blotting. In the present experiment, compared with controls, expressions of collagen type I (COL I), collagen type III (COL III), transforming growth factor (TGF)-β1, and tissue inhibitors of metalloproteinase (TIMP)-1 were all increased, but matrix metalloproteinase (MMP)-1 was reduced in CFB by Ang II treatment at both mRNA and protein levels, and these alterations were found reversed by miR-214 transfection. In vivo, an anterior transmural acute myocardial infarction (AMI) was created by occlusion of the left anterior descending coronary artery after Ad-pre-miR-214, Ad-anti-miR-214 or Ad-GFP was delivered separately. Four weeks after AMI, protein contents of COL I, COL III and TGF-β1 in tissue from border area were found increased after AMI, but impaired by overexpression of miR-214. While the expression of MMP-1 was increased by miR-214 stimulation but decreased by miR-214 inhibition. These results suggested that miR-214 exerts cardio-protective effects by inhibition of fibrosis and the inhibitory effect involves TGF-β1 suppression and MMP-1/TIMP-1 regulation. Anat Rec, 299:1348-1357, 2016. © 2016 Wiley Periodicals, Inc.

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The dynamic extracellular matrix: intervention strategies during heart failure and atherosclerosis

Cited by 120 publications

References 104 publications

Sodium tanshinone IIA sulfonate attenuates angiotensin II-induced collagen type I expression in cardiac fibroblasts in vitro

Sodium tanshinone IIA sulfonate attenuates angiotensin II-induced collagen type I expression in cardiac fibroblasts in vitro

Regulation of TGFβ1-mediated Collagen Formation by LOX-1

MicroRNA‐214 exerts a Cardio‐protective effect by inhibition of fibrosis

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