Effect of Transforming Growth Factor‐β1, Interleukin‐6, and Interferon‐γ on the Expression of Type I Collagen, Heat Shock Protein 47, Matrix Metalloproteinase (MMP)‐1 and MMP‐2 by Fibroblasts from Normal Gingiva and Hereditary Gingival Fibromatosis

Martelli‐Júnior, Hercílio; Cotrim, P.; Graner, Edgard; Sauk, John J.; Coletta, Ricardo D.

doi:10.1902/jop.2003.74.3.296

Cited by 88 publications

(88 citation statements)

References 61 publications

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“…Our results showed that IFN-g weakly reduces pro-collagen type I production, whereas it has no signifi cant effect on MMP-1 activation in HGF. Similar results have been shown in recent studies using 2 types of human fi broblasts [23,24]. Together, these data suggest that unlike IL-1b, IFN-g decreases type I collagen synthesis by human fi broblasts, however, it does not signifi cantly moderate the extracellular route of collagen digestion.…”

Section: Discussionsupporting

confidence: 90%

Interferon-γ inhibits collagen phagocytosis in human fibroblasts by inducing subcortical actin assembly and reducing ability of β1 integrin to bind to collagen

et al. 2006

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Although IFN-gamma does not appreciably moderate the extracellular route of collagen digestion by human fibroblasts, the reduced level of collagen phagocytosis by IFN-gamma in the cells may contribute to fibrosis in inflamed connective tissues. Further, IFN-gamma may decrease the binding of collagen and following phagocytosis in cells by inducing a subcortical actin assembly and reducing the ability of beta1 integrin to bind to collagen.

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Section: Discussionsupporting

confidence: 90%

Interferon-γ inhibits collagen phagocytosis in human fibroblasts by inducing subcortical actin assembly and reducing ability of β1 integrin to bind to collagen

et al. 2006

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“…Other included biomarkers that have not been mentioned above are markers in the field of connective tissue,41 lipids,42, 43 the immune system,44, 45, 46, 47, 48, 49, 50, 51 kidney function,52, 53 and hormones54, 55 (see Table 1). …”

Section: Resultsmentioning

confidence: 99%

Systematic Review of Circulating, Biomechanical, and Genetic Markers for the Prediction of Abdominal Aortic Aneurysm Growth and Rupture

Groeneveld

Meekel

Rubinstein

et al. 2018

JAHA

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BackgroundThe natural course of abdominal aortic aneurysms (AAA) is growth and rupture if left untreated. Numerous markers have been investigated; however, none are broadly acknowledged. Our aim was to identify potential prognostic markers for AAA growth and rupture.Methods and ResultsPotential circulating, biomechanical, and genetic markers were studied. A comprehensive search was conducted in PubMed, Embase, and Cochrane Library in February 2017, following Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines. Study selection, data extraction, and methodological quality assessment were conducted by 2 independent researchers. Plausibility of markers was based on the amount of publications regarding the marker (more than 3), pooled sample size (more than 100), bias risk and statistical significance of the studies. Eighty‐two studies were included, which examined circulating (n=40), biomechanical (n=27), and genetic markers (n=7) and combinations of markers (n=8). Factors with an increased expansion risk included: AAA diameter (9 studies; n=1938; low bias risk), chlamydophila pneumonia (4 studies; n=311; medium bias risk), S‐elastin peptides (3 studies; n=205; medium bias risk), fluorodeoxyglucose uptake (3 studies; n=104; medium bias risk), and intraluminal thrombus size (5 studies; n=758; medium bias risk). Factors with an increased rupture risk rupture included: peak wall stress (9 studies; n=579; medium bias risk) and AAA diameter (8 studies; n=354; medium bias risk). No meta‐analysis was conducted because of clinical and methodological heterogeneity.ConclusionsWe identified 5 potential markers with a prognostic value for AAA growth and 2 for rupture. While interpreting these data, one must realize that conclusions are based on small sample sizes and clinical and methodological heterogeneity. Prospective and methodological consonant studies are strongly urged to further study these potential markers.

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“…[17][18][19][20][21] The pathophysiologic mechanisms underlying HGF remain enigmatic; however, excessive accumulation of extracellular matrix components, particularly collagen type I, seem to contribute to the clinical-pathologic manifestations. [22][23][24] In a comparative study performed on normal gingiva and HGF fibroblasts, Martelli-Junior et al showed that the expression and production of type I collagen is significantly higher in fibroblasts from HGF than from normal gingiva. 24 They also demonstrated that addition of TGF-b1 and IL-6, which are produced in greater amounts by HGF fibroblasts, promoted an increase in type 1 collagen.…”

mentioning

confidence: 99%

“…[22][23][24] In a comparative study performed on normal gingiva and HGF fibroblasts, Martelli-Junior et al showed that the expression and production of type I collagen is significantly higher in fibroblasts from HGF than from normal gingiva. 24 They also demonstrated that addition of TGF-b1 and IL-6, which are produced in greater amounts by HGF fibroblasts, promoted an increase in type 1 collagen. Type 1 collagen is the major component of the extracellular matrix which is produced in principal by fibroblasts and TGF-b and IL-6 have crucial roles in promoting the synthesis of the collagen together with other growth factors.…”

mentioning

confidence: 99%

REST Final-Exon-Truncating Mutations Cause Hereditary Gingival Fibromatosis

Bayram

White

Elçioğlu

et al. 2017

The American Journal of Human Genetics

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Hereditary gingival fibromatosis (HGF) is the most common genetic form of gingival fibromatosis that develops as a slowly progressive, benign, localized or generalized enlargement of keratinized gingiva. HGF is a genetically heterogeneous disorder and can be transmitted either as an autosomal-dominant or autosomal-recessive trait or appear sporadically. To date, four loci (2p22.1, 2p23.3-p22.3, 5q13-q22, and 11p15) have been mapped to autosomes and one gene (SOS1) has been associated with the HGF trait observed to segregate in a dominant inheritance pattern. Here we report 11 individuals with HGF from three unrelated families. Whole-exome sequencing (WES) revealed three different truncating mutations including two frameshifts and one nonsense variant in RE1-silencing transcription factor (REST) in the probands from all families and further genetic and genomic analyses confirmed the WES-identified findings. REST is a transcriptional repressor that is expressed throughout the body; it has different roles in different cellular contexts, such as oncogenic and tumor-suppressor functions and hematopoietic and cardiac differentiation. Here we show the consequences of germline final-exontruncating mutations in REST for organismal development and the association with the HGF phenotype.

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Effect of Transforming Growth Factor‐β1, Interleukin‐6, and Interferon‐γ on the Expression of Type I Collagen, Heat Shock Protein 47, Matrix Metalloproteinase (MMP)‐1 and MMP‐2 by Fibroblasts from Normal Gingiva and Hereditary Gingival Fibromatosis

Cited by 88 publications

References 61 publications

Interferon-γ inhibits collagen phagocytosis in human fibroblasts by inducing subcortical actin assembly and reducing ability of β1 integrin to bind to collagen

Interferon-γ inhibits collagen phagocytosis in human fibroblasts by inducing subcortical actin assembly and reducing ability of β1 integrin to bind to collagen

Systematic Review of Circulating, Biomechanical, and Genetic Markers for the Prediction of Abdominal Aortic Aneurysm Growth and Rupture

REST Final-Exon-Truncating Mutations Cause Hereditary Gingival Fibromatosis

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