Impact of FGF1 on human periodontal ligament fibroblast growth, osteogenic differentiation and inflammatory reaction in vitro.

Einfluss von FGF1 auf Wachstum, osteogene Differenzierung und inflammatorische Stressreaktion humaner Parodontalligamentfibroblasten in vitro.

Journal

Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie
ISSN: 1615-6714
Titre abrégé: J Orofac Orthop
Pays: Germany
ID NLM: 9713484

Informations de publication

Date de publication:
Oct 2022
Historique:
received: 25 01 2021
accepted: 20 10 2021
pubmed: 8 12 2021
medline: 19 10 2022
entrez: 7 12 2021
Statut: ppublish

Résumé

To investigate in vitro the impact of fibroblast growth factor 1 (FGF1) in comparison to ascorbic acid (AscA) on human periodontal ligament fibroblast (HPdLF) growth, their osteogenic differentiation, and modulation of their inflammatory reaction to mechanical stress. The influence of different concentrations of FGF1 (12.5-200 ng/mL) on growth and proliferation of HPdLF cells was analyzed over 20 days by counting cell numbers and the percentage of Ki67-positive cells. Quantitative expression analysis of genes encoding the osteogenic markers alkaline phosphatase (ALPL), Runt-related transcription factor 2 (RUNX2), osteocalcin (OCN), and osteopontin (OSP), as well as the fibroblast markers vimentin (VIM) and fibroblast-specific protein 1 (FSP1), was performed after 2 and 20 days of cultivation. Metabolic activity was determined by MTT assay. For comparison with AscA, 50 ng/mL FGF1 was used for stimulation for 2 and 20 days. Cell number, percentage of Ki67-positive cells, and expression of osteoblast- and fibroblast-specific genes were examined. Alkaline phosphatase activity was visualized by NBT/BCIP and calcium deposits were stained with alizarin red. Cytokine (IL‑6, IL‑8, COX2/PGE2) expression and secretion were analyzed by qPCR and ELISA in 6 h mechanically compressed HPdLF cultured for 2 days with FGF1 or ascorbic acid. Higher concentrations of FGF1 promoted cell proliferation upon short-term stimulation, whereas prolonged treatment induced the expression of osteogenic markers even with low concentrations. AscA promotes cell growth more markedly than FGF1 in short-term cultures, whereas FGF1 induced osteogenic cell fate more strongly in long-term culture. Both factors induced an increased inflammatory response of HPdLF to mechanical compression. Our data suggest that FGF1 promotes an osteogenic phenotype of HPdLF and limits inflammatory response to mechanical forces compared to AscA. ZIELSETZUNG: In-vitro-Evaluation des Einflusses von Fibroblastenwachstumsfaktor 1 (FGF1) im Vergleich zu Ascorbinsäure (AscA) auf das Wachstum, das osteogene Differenzierungspotenzial und die inflammatorische Stressreaktion humaner Parodontalligamentfibroblasten (HPdLF). Der Einfluss von verschiedenen Konzentrationen von FGF1 (12,5–200 ng/ml) auf das Wachstum und die Proliferation von HPdLF-Zellen wurde über 20 Tage anhand von Zellzahlen und dem Anteil an Ki67-positiven Zellen analysiert. Die quantitative Expressionsanalyse von Genen, welche für die osteogenen Marker alkalische Phosphatase (ALPL), „runt-related transcription factor 2“ (RUNX2), Osteocalcin (OCN) und Osteopontin (OSP) sowie für die Fibroblastenmarker Vimentin (VIM) und „fibroblast-specific protein 1“ (FSP1) kodieren, wurde nach 2 und 20 Tagen Kultivierung durchgeführt. Die metabolische Aktivität wurde mittels MTT-Assay bestimmt. Für den Vergleich mit AscA wurde 50 ng/ml FGF1 zur Stimulation für 2 und 20 Tage verwendet. Die Zellzahl, der Anteil Ki67-positiver Zellen und die Expression von osteoblasten- und fibroblastenspezifischen Genen wurden untersucht. Die Aktivität der alkalischen Phosphatase wurde mittels NBT/BCIP visualisiert und Kalziumablagerungen mit Alizarin-Rot angefärbt. Die Expression und die Sezernierung von Zytokinen (IL‑6, IL‑8, COX2/PGE2) wurden mittels qPCR und ELISA in 6 h mechanisch komprimierten HPdLF analysiert, die 2 Tage mit FGF1 oder Ascorbinsäure kultiviert wurden. Höhere Konzentrationen von FGF1 förderten die Zellproliferation bei Kurzzeitstimulation, während bei längerer Behandlung auch mit niedrigen Konzentrationen die Expression osteogener Marker induziert wurde. AscA förderte das Zellwachstum in Kurzzeitkulturen deutlicher als FGF1, wohingegen FGF1 den osteogenen Phänotyp bei Langzeitkultivierung stärker hervorrief. Beide Faktoren induzierten eine erhöhte inflammatorische Reaktion von HPdLF auf mechanische Kompression. Unsere Daten deuten darauf hin, dass FGF1 den osteogenen Phänotyp von HPdLF bei Langzeitkultivierung fördert und die immunologische Stressreaktion auf mechanische Kräfte im Vergleich zu AscA mindert.

Autres résumés

Type: Publisher (ger)
ZIELSETZUNG: In-vitro-Evaluation des Einflusses von Fibroblastenwachstumsfaktor 1 (FGF1) im Vergleich zu Ascorbinsäure (AscA) auf das Wachstum, das osteogene Differenzierungspotenzial und die inflammatorische Stressreaktion humaner Parodontalligamentfibroblasten (HPdLF).

Identifiants

pubmed: 34874457
doi: 10.1007/s00056-021-00363-6
pii: 10.1007/s00056-021-00363-6
doi:

Substances chimiques

Core Binding Factor Alpha 1 Subunit 0
Interleukin-6 0
Interleukin-8 0
Ki-67 Antigen 0
S100 Calcium-Binding Protein A4 0
Vimentin 0
Fibroblast Growth Factor 1 104781-85-3
Osteocalcin 104982-03-8
Osteopontin 106441-73-0
Cyclooxygenase 2 EC 1.14.99.1
Alkaline Phosphatase EC 3.1.3.1
Dinoprostone K7Q1JQR04M
Ascorbic Acid PQ6CK8PD0R
Calcium SY7Q814VUP

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

42-55

Informations de copyright

© 2021. Springer Medizin Verlag GmbH, ein Teil von Springer Nature.

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Auteurs

Isabel Knaup (I)

Department of Orthodontics, RWTH Aachen University Hospital, Pauwelsstr. 30, 52074, Aachen, Germany. iknaup@ukaachen.de.

Judit Symmank (J)

Department of Orthodontics, Jena University Hospital, Jena, Germany.

Asisa Bastian (A)

Department of Orthodontics, RWTH Aachen University Hospital, Pauwelsstr. 30, 52074, Aachen, Germany.

Sabine Neuss (S)

Helmholtz Institute for Biomedical Engineering, BioInterface Group, RWTH Aachen University, Aachen, Germany.
Institute of Pathology, RWTH Aachen University Hospital, Aachen, Germany.

Thomas Pufe (T)

Department of Anatomy and Cell Biology, RWTH Aachen University Hospital, Wendlingweg 2, 52074, Aachen, Germany.

Collin Jacobs (C)

Department of Orthodontics, Jena University Hospital, Jena, Germany.

Michael Wolf (M)

Department of Orthodontics, RWTH Aachen University Hospital, Pauwelsstr. 30, 52074, Aachen, Germany.

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