The Comparative Role of Activator Protein 1 and Smad Factors in the Regulation of Timp-1 and MMP-1 Gene Expression by Transforming Growth Factor-β1

M, Hall; Young, David A.; Waters, Jasmine G.; Rowan, Andrew D.; Chantry, Andrew; Edwards, Dylan R.; Clark, Ian M.

doi:10.1074/jbc.m212334200

Cited by 221 publications

(196 citation statements)

References 50 publications

(53 reference statements)

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“…Wnt5a increased the promoter activity (Figure 5b). It was reported that the proximal AP-1 site at À72 is necessary for the phorbol ester-induced expression of MMP-1 (Hall et al, 2003). The basal reporter gene activity was decreased by introducing mutations in this area (AP-1 mut), and Wnt5a did not stimulate it (Figure 5b).…”

Section: Mechanism Of Wnt5a-induced Invasion By Pca Cellsmentioning

confidence: 90%

“…The MMP-1 promoter-luciferase constructs and pGEXaPAK-CRIB were provided by Dr I Clark (University of East Anglia, Norwich, UK) (Hall et al, 2003) and Dr K Kaibuchi (Nagoya University, Nagoya, Japan), respectively. DU145, LNCap and PC3 cells were obtained from American Type Culture Collection (Manassas, VA, USA) and were grown in RPMI-1640 medium supplemented with 10% fetal bovine serum.…”

Section: Materials and Chemicalsmentioning

confidence: 99%

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Wnt5a signaling is involved in the aggressiveness of prostate cancer and expression of metalloproteinase

et al. 2010

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Wnt5a is a representative ligand that activates the b-catenin-independent pathway in Wnt signaling. Although it has been reported that abnormal activation of the Wnt/ b-catenin-dependent pathway is often observed in human prostate cancer, the involvement of the b-catenin-independent pathway in this cancer is unclear. Abnormal expression of Wnt5a and b-catenin was observed in 27 (28%) and 49 (50%) of 98 prostate cancer cases, respectively, by immunohistochemical analyses. Simultaneous expression of Wnt5a and b-catenin was observed in only five cases, suggesting their exclusive expression. The positive detection of Wnt5a was correlated with high Gleason scores and biochemical relapse of prostate cancer, but that of b-catenin was not. Knockdown and overexpression of Wnt5a in human prostate cancer cell lines reduced and stimulated, respectively, their invasion activities, and the invasion activity required Frizzled2 and Ror2 as Wnt receptors. Wnt5a activated Jun-N-terminal kinase through protein kinase D (PKD) and the inhibition of PKD suppressed Wnt5a-dependent cell migration and invasion. In addition, Wnt5a induced the expression of metalloproteinase-1 through the recruitment of JunD to its promoter region. These results suggest that Wnt5a promotes the aggressiveness of prostate cancer and that its expression is involved in relapse after prostatectomy.

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Section: Mechanism Of Wnt5a-induced Invasion By Pca Cellsmentioning

confidence: 90%

Section: Materials and Chemicalsmentioning

confidence: 99%

Wnt5a signaling is involved in the aggressiveness of prostate cancer and expression of metalloproteinase

et al. 2010

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“…In the murine TIMP-1 gene, the AP1 site is located at À59 bp and is important in both basal and inducible TIMP-1 gene expression. 21 Many cytokines and matricellular factors influence MMP/TIMP expression through the NF-kB and AP-1 pathways. 22 Stimulation of rat cardiac fibroblasts with Ang II induces the production of both NF-kB and AP-1 transcription factors and is associated with an increase in collagen I production as well as a decrease in MMP-1 expression.…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone attenuates myocardial remodeling in spontaneously hypertensive rats

Hao

et al. 2011

Hypertens Res

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Rosiglitazone, an important peroxisome proliferator-activated receptor-c (PPAR-c) agonist, improves left ventricular (LV) hypertrophy in diet-induced hypercholesterolemic rats. However, the effects and underlying mechanisms of rosiglitazone on myocardial remodeling in spontaneous hypertension rats (SHRs) are unclear. Twenty male 8-week-old SHRs were randomly divided into two groups: one treated with oral saline (n¼10) and the other treated with rosiglitazone (5 mg kg À1 day À1 , n¼10). Ten age-matched Wistar-Kyoto rats were selected as a normal control group. Echocardiography, immunohistochemistry, real-time reverse transcriptase-PCR and western blot analysis were performed to assess the effects of rosiglitazone. After 16 weeks of treatment, LV hypertrophy was significantly attenuated by rosiglitazone (LV weight/body weight, 2.35±0.11 vs. 2.56 ± 0.14 mg g À1 ). According to the echocardiography results, thickening of the LV wall was reduced, and mid-wall fractional shortening was improved by rosiglitazone. Similarly, the excessive collagen deposition and upregulation of collagen I and collagen III seen in SHRs receiving saline were significantly attenuated in SHRs receiving rosiglitazone. In addition, rosiglitazone treatment increased the activity of matrix metalloproteinase-9 (MMP-9) and normalized the MMP-9/tissue inhibitor of metalloproteinase-1 ratio. Furthermore, activator protein-1 (AP-1) activation and nuclear factor-kappa B (NF-jB) expression were suppressed in the rosiglitazone-treated group. These results demonstrate that the PPAR-c agonist rosiglitazone had beneficial effects on myocardial remodeling in SHRs by way of decreasing AP-1 activation and NF-jB expression, which may help in further inhibiting transcription of the downstream genes involved in the pathogenesis of myocardial remodeling induced by hypertension.

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“…The phorbol myristate acetate (PMA) stimulates the expression and production of MMP-1 in human fibroblasts through the binding of the c-Jun factor to the AP-1 site of the MMP-1 promoter (25,26). Conversely, all-trans-or 9-cis-retinoic acid (RA) isomers reduce MMP-1 expression via the formation of a large repressor complex containing c-Jun that binds directly to the AP-1 site and apparently tethers the retinoid receptors (RARs and RXRs) to the complex (27).…”

Section: Mmp-1 Overexpression Is a Specific Trait Of Ttd/xp-d Dermal mentioning

confidence: 99%

TFIIH-dependent MMP-1 overexpression in trichothiodystrophy leads to extracellular matrix alterations in patient skin

Arseni

Lanzafame

Compe

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Mutations in the XPD subunit of the DNA repair/transcription factor TFIIH result in distinct clinical entities, including the cancerprone xeroderma pigmentosum (XP) and the multisystem disorder trichothiodystrophy (TTD), which share only cutaneous photosensitivity. Gene-expression profiles of primary dermal fibroblasts revealed overexpression of matrix metalloproteinase 1 (MMP-1), the gene encoding the metalloproteinase that degrades the interstitial collagens of the extracellular matrix (ECM), in TTD patients mutated in XPD compared with their healthy parents. The defect is observed in TTD and not in XP and is specific for fibroblasts, which are the main producers of dermal ECM. MMP-1 transcriptional up-regulation in TTD is caused by an erroneous signaling mediated by retinoic acid receptors on the MMP-1 promoter and leads to hypersecretion of active MMP-1 enzyme and degradation of collagen type I in the ECM of cell/tissue systems and TTD patient skin. In agreement with the well-known role of ECM in eliciting signaling events controlling cell behavior and tissue homeostasis, ECM alterations in TTD were shown to impact on the migration and wound-healing properties of patient dermal fibroblasts. The presence of a specific inhibitor of MMP activity was sufficient to restore normal cell migration, thus providing a potential approach for therapeutic strategies. This study highlights the relevance of ECM anomalies in TTD pathogenesis and in the phenotypic differences between TTD and XP.T he extracellular matrix (ECM) is a complex structural network that surrounds and supports cells within connective tissues. It generally includes three major types of macromolecules: fibrous proteins (collagens and elastic fibers), glycoproteins (such as fibronectins and laminins), and glycosaminoglycans/ proteoglycans. The type, amount and composition of the ECM give tissues their unique physical and biological properties (1). Notably, the ECM is not only a structural scaffold but also exhibits important functional roles in controlling key cellular events (e.g., adhesion, migration, proliferation, differentiation, and survival) involved in tissue homeostasis, development, inflammation, and tissue repair (2, 3). Thus, inherited or acquired structural alterations as well as metabolic disturbances of the ECM may cause cellular and tissue changes leading to the onset and progression of specific disorders, such as those affecting the connective tissues (osteogenesis imperfecta, Ehlers-Danlos syndrome, and Marfan's syndrome) or demanding ECM degradation (tumor invasion and metastasis) (4, 5). Recently, a reduced synthesis of the ECM component collagen type VI (COL6) was shown in confluent fibroblast cultures from patients with trichothiodystrophy [TTD; Online Mendelian Inheritance in Man (OMIM) #601675] (6), an autosomal recessive disorder characterized by symptoms affecting several tissues and organs (7). The most relevant features of TTD are hair abnormalities, ichthyotic skin, physical and mental retardation, neurodegeneration, and sign...

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The Comparative Role of Activator Protein 1 and Smad Factors in the Regulation of Timp-1 and MMP-1 Gene Expression by Transforming Growth Factor-β1

Cited by 221 publications

References 50 publications

Wnt5a signaling is involved in the aggressiveness of prostate cancer and expression of metalloproteinase

Wnt5a signaling is involved in the aggressiveness of prostate cancer and expression of metalloproteinase

Rosiglitazone attenuates myocardial remodeling in spontaneously hypertensive rats

TFIIH-dependent MMP-1 overexpression in trichothiodystrophy leads to extracellular matrix alterations in patient skin

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