Effect of adenovirus-mediated overexpression of decorin on metalloproteinases, tissue inhibitors of metalloproteinases and cytokines secretion by human gingival fibroblasts

Zen, Ayman Al Haj; Lafont, Antoine; Durand, Éric; Brasselet, Camille; Lemarchand, Patricia; Godeau, Gaston; Gogly, Bruno

doi:10.1016/s0945-053x(03)00018-0

Cited by 43 publications

(35 citation statements)

References 20 publications

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“…Proteoglycans with their highly diverse GAG chain glycosylation are a major part of the ECM and exhibit multiple functions, e.g. modulation of growth factor activities, regulation of collagen fibrillogenesis, or tensile strength [31][32][33]. Interestingly, we could observe an increase in myocardial mRNA levels of MMP-2 and -9 in rats with DCM ( Fig.…”

Section: Discussionmentioning

confidence: 76%

Small interfering RNA therapy against carbohydrate sulfotransferase 15 inhibits cardiac remodeling in rats with dilated cardiomyopathy

Watanabe

Arumugam

Sreedhar

et al. 2015

Cellular Signalling

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Carbohydrate sulfotransferase 15 (CHST15) is a sulfotransferase responsible for biosynthesis of chondroitin sulfate E (CS-E), which plays important roles in numerous biological events such as biosynthesis of proinflammatory cytokines. However, the effects of CHST15 siRNA in rats with chronic heart failure (CHF) after experimental autoimmune myocarditis (EAM) have not yet been investigated. CHF was elicited in Lewis rats by immunization with cardiac myosin, and after immunization, the rats were divided into two groups and treated with either CHST15 siRNA (2μg/week) or vehicle. Age matched normal rats without immunizations were also included in this study. After 7weeks of treatment, we investigated the effects of CHST15 siRNA on cardiac function, proinflammatory cytokines, and cardiac remodeling in EAM rats. Myocardial functional parameters measured by hemodynamic and echocardiographic studies were significantly improved by CHST15 siRNA treatment in rats with CHF compared with that of vehicle-treated CHF rats. CHST15 siRNA significantly reduced cardiac fibrosis, and hypertrophy and its marker molecules (left ventricular (LV) mRNA expressions of transforming growth factor beta1, collagens I and III, and atrial natriuretic peptide) compared with vehicle-treated CHF rats. CHF-induced increased myocardial mRNA expressions of proinflammatory cytokines [interleukin (IL)-6, IL-1β], monocyte chemoattractant protein-1, and matrix metalloproteinases (MMP-2 and -9), and CHST15 were also suppressed by the treatment with CHST15 siRNA. Western blotting study has confirmed the results obtained from mRNA analysis as CHST15 siRNA treated rats expressed reduced levels of inflammatory and cardiac remodeling marker proteins. Our results demonstrate for the first time, that CHST15 siRNA treatment significantly improved LV function and ameliorated the progression of cardiac remodeling in rats with CHF after EAM.

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Section: Discussionmentioning

confidence: 76%

Small interfering RNA therapy against carbohydrate sulfotransferase 15 inhibits cardiac remodeling in rats with dilated cardiomyopathy

Watanabe

Arumugam

Sreedhar

et al. 2015

Cellular Signalling

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“…Moreover the relative decrease in two major matrix metalloproteases, MMP-2 and MMP-9, and the concurrent increase in the hepatic levels of two major MMP inhibitors, TIMP-1 and PAI-1, indicated an impaired clearance of the deposited ECM (Baghy et al 2011). An adenovirus-mediated direct stimulatory effect of decorin on metalloproteases has been previously described (Al Haj Zen et al 2003;Dong et al 2008). On the other hand, TIMP-1 as well as PAI-1 levels can also be stimulated by TGF-β1 (Kutz et al 2001;Akool el et al 2005).…”

Section: Effects Of Decorin On Tgf-β1 Action In Liver Fibrosismentioning

confidence: 99%

Decorin–TGFβ Axis in Hepatic Fibrosis and Cirrhosis

Baghy

Iozzo

Kovalszky

2012

J Histochem Cytochem.

146

128

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Hepatic fibrosis and cirrhosis are worldwide health care problems, especially in regions with a high rate of hepatitis infection. As these diseases affect a major part of the human population, the search for antifibrotic therapies has a high priority in medical research. Transforming growth factor β1 (TGF-β1) is one of the most powerful profibrotic cytokines. Thus, blocking TGF-β1 activity by natural inhibitors represents a valid and logical strategy to combat hepatic fibrosis. One of the natural inhibitors of TGF-β1 is decorin, a small leucine-rich proteoglycan that binds with high affinity to this cytokine and prevents its interaction with pro-fibrotic receptors. Recent evidence has shown that decorin has a protective role in liver fibrogenesis insofar as its genetic ablation in mice leads to enhanced matrix deposition, impaired matrix degradation, and “activation” of hepatic stellate cells, the main producers of fibrotic tissue. Moreover, TGF-β1 exerts a stronger effect when functional decorin is absent. These data provide robust genetic evidence for a direct role of endogenous decorin in preventing and retarding hepatic fibrosis. Thus, boosting the endogenous production of decorin or systemic delivery of recombinant decorin could represent an additional therapeutic modality against hepatic fibrosis.

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“…Five human gingival and 3 dermal fibroblasts (hGF and hDF) cultures were obtained from gingival and dermal explants as previously described 17 and incorporated in collagen lattices. 18 …”

Section: Human Cell Culturementioning

confidence: 99%

Preservation of Rabbit Aorta Elastin From Degradation by Gingival Fibroblasts in an Ex Vivo Model

Gogly

Naveau

Fournier

et al. 2007

ATVB

Self Cite

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Objective-Embryo-like gingival healing properties are attributed to the gingival fibroblast (GF) and could be used as a model for other types of healing dysfunctions. Abdominal aortic aneurysm (AAA) formation is associated with elastin degradation and increase in matrix metalloproteinase (MMP)-9 activity. We aimed to validate the concept of using GF healing properties in arteries. Methods and Results-We evaluated MMP-9 and its tissue inhibitor (TIMP-1) in rabbit aortic rings cultured in collagen gels with or without GFs and observed throughout 21 days. We also performed cocultures of human smooth muscle cells (hSMCs) with either gingival, dermal, or adventitial fibroblasts, and alone (control). In control arteries, elastic fibers became spontaneously sparse. In presence of GFs, elastic fibers were preserved. There was a dramatically reduced protein level of MMP-9 in coculture of aorta and GFs, in contrast with control aorta. MMP-9 expression was unaffected by GFs. MMP-9 inhibition was related to increased TIMP-1 secretion, TIMP-1 forming a complex with MMP-9. Cell cocultures of hSMC with GFs showed similar results. Dermal and adventitial fibroblasts did not affect MMP-9. Conclusions-Elastic fiber degradation was specifically preserved by GFs via reduction of MMP-9 protein level by increasing TIMP-1 synthesis. Vascular transfer of gingival fibroblasts could be a promising approach to treat AAA.

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Effect of adenovirus-mediated overexpression of decorin on metalloproteinases, tissue inhibitors of metalloproteinases and cytokines secretion by human gingival fibroblasts

Cited by 43 publications

References 20 publications

Small interfering RNA therapy against carbohydrate sulfotransferase 15 inhibits cardiac remodeling in rats with dilated cardiomyopathy

Small interfering RNA therapy against carbohydrate sulfotransferase 15 inhibits cardiac remodeling in rats with dilated cardiomyopathy

Decorin–TGFβ Axis in Hepatic Fibrosis and Cirrhosis

Preservation of Rabbit Aorta Elastin From Degradation by Gingival Fibroblasts in an Ex Vivo Model

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