The Nuclear Receptor Corepressor SMRT Inhibits Interstitial Collagenase (MMP-1) Transcription through an HRE-Independent Mechanism

Schroen, Daniel J.; Chen, J.Don; Vincenti, Matthew P.; Brinckerhoff, Constance E.

doi:10.1006/bbrc.1997.7073

Cited by 13 publications

(7 citation statements)

References 49 publications

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“…32 Furthermore, MMP-1 gene expression by synovial fibroblasts was found to be inhibited through the nuclear receptor SMRT (silencing mediator for retinoid and thyroid hormone receptors). 33 In this study, we could not detect any significant inhibition in the production of MMP-2, -1, or -9, indicating that MMP production may be regulated differently in various cell types. This suggests a possibility that the transcription of MMPs may be differently regulated in various cell types.…”

Section: Effect Of Tzd On Cancer Cell Adhesion To Ecm Proteinscontrasting

confidence: 54%

Decreased Synthesis of Matrix Metalloproteinase-7 and Adhesion to the Extracellular Matrix Proteins of Human Colon Cancer Cells Treated with Troglitazone

Sunami¹,

Tsuno²,

Kitayama³

et al. 2002

Surgery Today

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Section: Effect Of Tzd On Cancer Cell Adhesion To Ecm Proteinscontrasting

confidence: 54%

Decreased Synthesis of Matrix Metalloproteinase-7 and Adhesion to the Extracellular Matrix Proteins of Human Colon Cancer Cells Treated with Troglitazone

Sunami¹,

Tsuno²,

Kitayama³

et al. 2002

Surgery Today

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“…RARβ can repress in the absence of ligand, suggesting that co-repressors may be involved in transrepression of the MMP-1 promoter. This hypothesis is supported by recent work demonstrating that the nuclear hormone receptor SMRT can repress vsrc-induced MMP-1 transcription through sequences in the proximal MMP-1 promoter in the absence of ligand [52]. These findings suggest that antagonism of the v-src signaling pathway that leads to MMP-1 transcription may be an important step in tumor suppression.…”

Section: Discussionsupporting

confidence: 55%

“…Taken together, these data show that RA, working through RARs, is an effective inhibitory signal for oncogene-driven MMP-1 transcription. Furthermore, the RARα and RARβ isotypes are capable of ligand-independent suppression, possibly by recruitment of co-repressor proteins to the MMP-1 promoter [34,52].…”

Section: Inhibition Of V-src-induced Mmp-1 Transcription By Ra and Rarsmentioning

confidence: 99%

v-src activation of the collagenase-1 (matrix metalloproteinase-1) promoter through PEA3 and STAT: Requirement of extracellular signal-regulated kinases and inhibition by retinoic acid receptors

et al. 1998

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Collagenase-1 (matrix metalloproteinase-1 (MMP-1)) degrades the extracellular matrix and enhances the invasive phenotype of tumor cells. v-src activated MMP-1 transcription through a series of elements in the proximal promoter, including the E2BP (nt -172), polyoma virus enhancer A3 (PEA3) (nt -94), activator protein-1 (AP-1) (nt -72), and signal transducer and activator of transcription (STAT) (nt -57) consensus sites. Of these sites, PEA3 and STAT contributed specifically to induction by v-src, whereas the remaining elements were also involved in induction by the phorbol ester phorbol myristate acetate (PMA). However, in contrast to MMP-1 induction by PMA, an AP-1 site located at nt -186 did not contribute to v-src induction. These results suggest divergence of the tyrosine kinase- and protein kinase C-dependent pathways with respect to MMP-1 transcription. v-src induced MMP-1 through mitogen-activated protein kinases, with extracellular signal-regulated kinases playing a larger role than c-jun N-terminal kinase. Retinoic acid, which inhibits the progression of certain cancers, repressed v-src-induced MMP-1 transcription. Constitutive expression of retinoic acid receptors (RARs) alpha or beta, but not gamma, or of retinoid X receptor alpha, repressed v-src-induced collagenase-1 transcription. We concluded that oncogenic induction of MMP-1 by v-src depends on signaling pathways and cis-acting sequences that are distinct from those involved in phorbol ester activation. Furthermore, v-src induction of MMP-1 may, by acting in concert with other genes, enhance matrix degradation and tumor progression, and retinoic acid and RARs may antagonize this induction in an RAR type-specific manner.

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“…While it has been identified that myocardial overexpression of aldosterone induces production of fibrotic proteins such as collagen (87,342), whether and to what degree aldosterone influences MMP transcription directly remains unknown. There is no direct evidence to date to suggest that a MMP promoter region contains a hormone response element (HRE) (389). Although it has been demonstrated that other steroids can modulate MMP expression, the effects of these steroids on the transcriptional regulation are likely due to indirect mechanisms of action (94,223 ET is another bioactive molecule that likely contributes to the adverse myocardial remodeling process.…”

Section: Modification Of Mmp Transcription By Prototypical Stimulimentioning

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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The Nuclear Receptor Corepressor SMRT Inhibits Interstitial Collagenase (MMP-1) Transcription through an HRE-Independent Mechanism

Cited by 13 publications

References 49 publications

Decreased Synthesis of Matrix Metalloproteinase-7 and Adhesion to the Extracellular Matrix Proteins of Human Colon Cancer Cells Treated with Troglitazone

Decreased Synthesis of Matrix Metalloproteinase-7 and Adhesion to the Extracellular Matrix Proteins of Human Colon Cancer Cells Treated with Troglitazone

v-src activation of the collagenase-1 (matrix metalloproteinase-1) promoter through PEA3 and STAT: Requirement of extracellular signal-regulated kinases and inhibition by retinoic acid receptors

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

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