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Abstract
BackgroundBasic fibroblast growth factor (bFGF) regulates maintenance of stemness and modulation of osteo/odontogenic differentiation and mineralization in stem cells from human exfoliated deciduous teeth (SHEDs). Mineralization in the bones and teeth is in part controlled by pericellular levels of inorganic phosphate (Pi), a component of hydroxyapatite, and inorganic pyrophosphate (PPi), an inhibitor of mineralization. The progressive ankylosis protein (gene ANKH; protein ANKH) and ectonucleotide pyrophosphatase phosphodiesterase 1 (ENPP1/ENPP1) increase PPi and inhibit mineralization, while tissue-nonspecific alkaline phosphatase (ALPL; TNAP) is a critical pro-mineralization enzyme that hydrolyzes PPi. We hypothesized that regulation by bFGF of mineralization in SHEDs occurs by modulation of Pi/PPi-associated genes.MethodsCells were isolated from human exfoliated deciduous teeth and characterized for mesenchymal stem cell characteristics. Cells were treated with bFGF, and the osteogenic differentiation ability was determined. The mRNA expression was evaluated using real-time polymerase chain reaction. The mineralization was examined using alizarin red S staining.ResultsCells isolated from primary teeth expressed mesenchymal stem cell markers, CD44, CD90, and CD105, and were able to differentiate into osteo/odontogenic and adipogenic lineages. Addition of 10 ng/ml bFGF to SHEDs during in vitro osteo/odontogenic differentiation decreased ALPL mRNA expression and ALP enzyme activity, increased ANKH mRNA, and decreased both Pi/PPi ratio and mineral deposition. Effects of bFGF on ALPL and ANKH expression were detected within 24 h. Addition of 20 mM fibroblast growth factor receptor (FGFR) inhibitor SU5402 revealed the necessity of FGFR-mediated signaling, and inclusion of 1 μg/ml cyclohexamide (CHX) implicated the necessity of protein synthesis for effects on ALPL and ANKH. Addition of exogenous 10 μm PPi inhibited mineralization and increased ANKH, collagen type 1a1 (COL1A1), and osteopontin (SPP1) mRNA, while addition of exogenous Pi increased mineralization and osterix (OSX), ANKH, SPP1, and dentin matrix protein 1 (DMP1) mRNA. The effects of PPi and Pi on mineralization could be replicated by short-term 3- and 7-day treatments, suggesting signaling effects in addition to physicochemical regulation of mineral deposition.ConclusionThis study reveals for the first time the effects of bFGF on Pi/PPi regulators in SHEDs and implicates these factors in how bFGF directs osteo/odontogenic differentiation and mineralization by these cells.
Highlights
Basic fibroblast growth factor regulates maintenance of stemness and modulation of osteo/ odontogenic differentiation and mineralization in stem cells from human exfoliated deciduous teeth (SHEDs)
This study reveals for the first time the effects of Basic fibroblast growth factor (bFGF) on Inorganic phosphate (Pi)/phosphate (Pi) and pyrophosphate (PPi) regulators in SHEDs and implicates these factors in how bFGF directs osteo/odontogenic differentiation and mineralization by these cells
Stem cells isolated from human exfoliated deciduous teeth (SHEDs) were reported in 2003 [5]
Summary
Basic fibroblast growth factor (bFGF) regulates maintenance of stemness and modulation of osteo/ odontogenic differentiation and mineralization in stem cells from human exfoliated deciduous teeth (SHEDs). Basic fibroblast growth factor (bFGF; known as FGF2) is a member of the fibroblast growth factor family of related signaling molecules crucial for development, maintenance, and repair of tissues While it regulates various cell processes including proliferation, migration, and differentiation, bFGF controls maintenance of stemness in human stem cells [1, 2]. The appeal of these postnatal mesenchymal stem cells (MSCs) is that they can be obtained non-invasively (isolated after natural exfoliation of primary teeth) and show the multipotent ability to differentiate into osteogenic, adipogenic, and neurogenic lineages [6] They are considered to be MSCs based on known developmental processes, SHEDs exhibit novel characteristics compared with bone marrow-derived MSCs, possibly due in part to their origin from cranial neural crest-derived ectomesenchyme and/or different patterns of signaling that occur in the craniofacial-dental region compared to the postcranial skeleton [5]
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