1999
DOI: 10.1007/s004410051374
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Differential in vitro phenotype pattern, transforming growth factor-β 1 activity and mRNA expression of transforming growth factor-β 1 in Apert osteoblasts

Abstract: The phenotype of Apert osteoblasts differs from that of normal osteoblasts in the accumulation of macromolecules in the extracellular matrix. Apert osteoblasts increase type I collagen, fibronectin and glycosaminoglycans secretion compared with normal osteoblasts. Because the extracellular matrix macromolecule accumulation is greatly modulated by transforming growth factor-beta(1), we examined the ability of normal and Apert osteoblasts to secrete transforming growth factor-beta(1) by CCL-64 assay and to produ… Show more

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Cited by 23 publications
(13 citation statements)
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“…Quantitative and qualitative alterations of GAG may be induced by modifying the extracellular environment that alters connective tissue cell metabolism. [38][39][40][41][42][43][44] Therefore, any variation in GAG composition can influence the tissue's state of health. Both the whole appliance and the single components of the appliance reduced the cellular and extracellular accumulation of GAG.…”
Section: Discussionmentioning
confidence: 99%
“…Quantitative and qualitative alterations of GAG may be induced by modifying the extracellular environment that alters connective tissue cell metabolism. [38][39][40][41][42][43][44] Therefore, any variation in GAG composition can influence the tissue's state of health. Both the whole appliance and the single components of the appliance reduced the cellular and extracellular accumulation of GAG.…”
Section: Discussionmentioning
confidence: 99%
“…One factor may be the imbalance between growth factor beta 1 (TGF A1) and basic fibroblast growth factor (FGF-b) in the extracellular matrix of Apert calvaria. 42 Another possible explanation is the lower interleukins (IL1 and IL6) noted in Apert periosteal fibroblasts. 43 The extracellular matrix of the calvaria of Crouzon patients also show increased type I collagen (similar to Apert syndrome).…”
Section: Fibronectin and Neural Crest Cellsmentioning
confidence: 99%
“…The observed imbalance in the production of ILs suggests that ILs could be the natural autocrine regulators of ECM production in Apert fibroblasts. Since TGF-β1 is able to modulate ECM macromolecule accumulation in fibroblasts (Bodo et al, 1999b), and a variety of osteoblast activities (Janssens et al, 2005), we also analysed its expression and secretion which resulted both increased in Apert osteoblasts in vitro (Locci et al, 1999). Moreover, the level of TGF-β1 was decreased by the addition of FGF2.…”
Section: Apert Syndromementioning
confidence: 99%