TGFβ Isoforms and Decorin Gene Expression are Modified in Fibroblasts Obtained from Non-syndromic Cleft Lip and Palate Subjects

Bodo, Maria; Baroni, Tiziano; Becchetti, Ennio; Bellucci, Catia; Pezzetti, Furio; Conte, Carmela; Evangelisti, R.; Carinci, Paolo

doi:10.1177/00220345990780120401

Cited by 29 publications

(31 citation statements)

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“…In previous in vitro studies on human CLP-SP fibroblasts, we showed marked phenotype alterations in GAG and collagen production as well as abnormal growth factor expression and aberrant cross-talk between TGF-β3 and IL-6 (39)(40)(41).…”

Section: Discussionmentioning

confidence: 75%

“…Our results demonstrate a low level of TGF-β3 transcription in N-SP cells and a modest but significantly higher level in CLP-SP cells. The low level of transcription could explain our failure to detect TGF-β3 mRNA in a previous work using a less sensitive technique (40). Nevertheless, the same study had demonstrated upregulated TGF-β3 protein secretion in CLP-SP cells, and adding TGF-β3 increased accumulation of ECM molecules.…”

Section: Discussionmentioning

confidence: 80%

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Retinoic Acid, GABA-ergic, and TGF-β Signaling Systems Are Involved in Human Cleft Palate Fibroblast Phenotype

Baroni

Bellucci

Lilli

et al. 2006

Mol Med

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During embryogenesis, a complex interplay between extracellular matrix (ECM) molecules, regulatory molecules, and growth factors mediates morphogenetic processes involved in palatogenesis. Transforming growth factor-β (TGF-β), retinoic acid (RA), and γ-aminobutyric acid (GABA)ergic signaling systems are also potentially involved. Using ]methionine incorporation, anion exchange chromatography, semiquantitative radioactive RT-PCR, and a TGF-β binding assay, we aimed to verify the presence of phenotypic differences between primary cultures of secondary palate (SP) fibroblasts from 2-year-old subjects with familial nonsyndromic cleft lip and/or palate (CLP-SP fibroblasts) and age-matched normal SP (N-SP) fibroblasts. The effects of RA-which, at pharmacologic doses, induces cleft palate in newborns of many species-were also studied. We found an altered ECM production in CLP-SP fibroblasts that synthesized and secreted more glycosaminoglycans (GAGs) and fibronectin (FN) compared with N-SP cells. In CLP-SP cells, TGF-β3 mRNA expression and TGF-β receptor number were higher and RA receptor-α (RARA) gene expression was increased. Moreover, we demonstrated for the first time that GABA receptor (GABRB3) mRNA expression was upregulated in human CLP-SP fibroblasts. In N-SP and CLP-SP fibroblasts, RA decreased GAG and FN secretion and increased TGF-β3 mRNA expression but reduced the number of TGF-β receptors. TGF-β receptor type I mRNA expression was decreased, TGF-β receptor type II was increased, and TGF-β receptor type III was not affected. RA treatment increased RARA gene expression in both cell populations but upregulated GABRB3 mRNA expression only in N-SP cells. These results show that CLP-SP fibroblasts compared with N-SP fibroblasts exhibit an abnormal phenotype in vitro and respond differently to RA treatment, and suggest that altered crosstalk between RA, GABAergic, and TGF-β signaling systems could be involved in human cleft palate fibroblast phenotype.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 80%

Retinoic Acid, GABA-ergic, and TGF-β Signaling Systems Are Involved in Human Cleft Palate Fibroblast Phenotype

Baroni

Bellucci

Lilli

et al. 2006

Mol Med

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“…The role of transforming growth factor alpha (TGF-A), mapping on 2p13, was taken into account in the CL±P onset, in light of its contribution in cell proliferation, differentiation and development. Some studies reported an association between TGF alpha and CL±P, but some others did not reply this result (25,26). Another positive association was found out between markers on chromosome region 19q13.2 and orofacial cleft malformation (27).…”

Section: Human Genetic Factorsmentioning

confidence: 96%

New Insights in Orofacial Cleft: Epidemiological and Genetic Studies on Italian Samples

Tettamanti

Avantaggiato

Nardone

et al. 2017

ORL

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SUMMARYCleft of the lip and/or palate (CL±P) is the most common congenital craniofacial anomaly affecting around 1 in 700 live births worldwide. Clefts of the human face can be classified anatomically as cleft lip only (CL), cleft palate only (CP), cleft lip and palate (CLP) or a combined group of cleft lip with or without cleft palate (CL±P), based on differences in embryologic development. CL±P has a genetic base and several linkage and association analyses have been performed in order to obtain important information about the role of candidate genes in its onset; not less important are gene-environment interactions that play an increasing role in its aetiology. In CL±P, several loci have been seen associated with the malformation, and, in some cases, a specific gene mapping in a locus has also been identified as susceptibility factor. In CP, one gene has been found, but many more are probably involved. In this short review the genetic studies carried out on CL±P, and the interaction with environmental factors (alcohol, smoking, drugs) are discussed.

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“…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%

“…We studied (Bodo et al, 1999b) TGF-α, TGF-β, and TGF-β3 expressions and their effects on ECM macromolecule production of normal and cleft palatal fibroblasts in vitro, to investigate the mechanisms by which the phenotypic modulation of fibroblasts occurs during the cleft palate process. TGF-β isoforms and ECM components were dif-P. Carinci et al ferently expressed and were correlated to the CLP phenotype.…”

Section: Non-syndromic Clpmentioning

confidence: 99%

The Fathers of Italian Histology

ISH¹

2009

Eur J Histochem

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Subscriptions, cancellations, business correspondence and any enquiries must be sent to the Tipografia PIME Editrice srl, Pavia, Italy. Cancellations must be received before the end of September to take effect at the end of the same year.No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means (electronic, electrostatic, magnetic type, mechanical, photocopying or otherwise) without written permission by the Publishers.Reg. Tribunale di Pavia n. 289/23.2.1984. Supported by the Ministero per i Beni e le Attività Culturali, Italy as a publication of high cultural value.Associato all'USPI Unione Stampa Periodica Italiana Disclaimer. Whilst every effort is made by the publishers and the editorial board to see that no inaccurate or misleading data, opinion or statement appears in this journal, they wish to make it clear that the data and opinions appearing in the articles or advertisements herein are the responsibility of the contributor or advisor concerned. Accordingly, the publisher, the editorial board and their respective employees, officers and agents accept no liability whatsoever for the consequences of any inaccurate or misleading data, opinion or statement. The Journal publishes original papers, technical reports, letters to the editor, review articles concerning investigations performed with the aid of biophysical, biochemical, molecular-biological, enzymatic, immunohistochemical, cytometric, and image analysis techniques. Areas of particular interest to the European Journal of Histochemistry include: -functional cell and tissue biology in animals and plants; -cell differentiation and death; -cell-cell interaction and molecular trafficking; -biology of cell development and senescence; -nerve and muscle cell biology; -cellular basis of diseases During this period, Carlo Rizzoli established the experimental approach for the study of the molecular basis of cell differentiation in vitro, anticipating some aspects of the present investigation on the potentiality of stem cells. Furthermore, Carlo Rizzoli was one of the first Italian scientists to publish its scientific reports in large-diffusion international journals, thus contributing to the world-wide diffusion of the seminal studies on the in vitro cell differentiation models. Editor-in-ChiefIn 1961, Carlo Rizzoli became Professor of Histology and general embryology and, since 1964 to 1999, Director of the Institute of Histology at the University of Bologna.The initial steps of this undertaking were challenging, since in 1963, following the recruitment of Oliviero Mario Olivo at the Chair of Human Anatomy, the facilities of the Institute of Histology were almost nonexistent. In few years, however, Carlo Rizzoli was able to organize an efficient research group of motivated young collaborators that included Paolo Carinci, Lia Guidotti, Francesco Antonio Manzoli, capable of introducing original and seminal lines of research into the national and international histological arena. In this way, a numb...

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TGFβ Isoforms and Decorin Gene Expression are Modified in Fibroblasts Obtained from Non-syndromic Cleft Lip and Palate Subjects

Cited by 29 publications

References 31 publications

Retinoic Acid, GABA-ergic, and TGF-β Signaling Systems Are Involved in Human Cleft Palate Fibroblast Phenotype

Retinoic Acid, GABA-ergic, and TGF-β Signaling Systems Are Involved in Human Cleft Palate Fibroblast Phenotype

New Insights in Orofacial Cleft: Epidemiological and Genetic Studies on Italian Samples

The Fathers of Italian Histology

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