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Review of the role of basic fibroblast growth factor in dental tissue-derived mesenchymal stem cells

Nunthawan Nowwarote
Nunthawan Nowwarote
, 
Chenphop Sawangmake
Chenphop Sawangmake
, 
Prasit Pavasant
Prasit Pavasant
 y 
Thanaphum Osathanon
Thanaphum Osathanon
   | 31 ene 2017
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Article Category: Review article
Publicado en línea: 31 ene 2017
Páginas: 271 - 283
DOI: https://doi.org/10.5372/1905-7415.0903.395
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© 2015 Nunthawan Nowwarote, Chenphop Sawangmake, Prasit Pavasant, Thanaphum Osathanon
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Figure 1

bFGF intracellular signaling. Activation by receptor autophosphorylation triggers diverse signaling cascades, including the Ras/ mitogen-activated protein kinase (MAPK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI-3 kinase)/protein kinase B (Akt), phospholipase C (PLC)-g/Ca2 and the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways. Phosphorylation of the docking protein, fibroblast growth factor receptor substrate 2 (FRS2) is followed by growth factor receptor-bound protein 2 (Grb2) activation, which in turns activates either the Ras/MAPK cascade via Son of Sevenless (SOS), or the PI-3 kinase/Akt pathway via Grb2-associated-binding protein 1 (Gab1). PI-3 kinase can also be activated directly by tyrosine phosphorylation or alternatively by Ras1. The other main transduction pathway involves PLC. The Src homology 2 (SH2) domain of the PLC interacts directly with the receptor leading to the hydrolysis of phosphatidyl-inositol-4,5-diphosphate (PIP2) to inositol-1,4,5-triphophate (IP-3) and diacylglycerol (DAG). Inositol-1,4,5-triphosphate (IP-3) releases Ca2+ from the endoplasmic reticulum (ER), while DAG activates protein kinase C (PKC) that in turn can activate the noncanonical planar cell polarity (PCP) pathway and RAF proto-oncogene serine/threonine-protein kinase (Raf1). Feedback inhibitors such as dual specificity phosphatase 6 (Dusp6)/mitogen-activated protein kinase phosphatase-3 (MKP-3), sprouty protein (Spry), FRS2a, sprouty-related, EVH1 domain-containing protein (Spred), and Sef involved in signal attenuation, and enhancers such as fibronectin leucine rich transmembrane protein 3 (XFLRT3) can also contribute to the overall levels of bFGF signaling. HSPGs, heparin sulphate proteoglycans; EMT, epithelial-to-mesenchymal transition; P, phosphorylation (modified from Villegas et al., 2010) [110] □ 2010 Wiley-Liss, Inc. with permission for reuse.
bFGF intracellular signaling. Activation by receptor autophosphorylation triggers diverse signaling cascades, including the Ras/ mitogen-activated protein kinase (MAPK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI-3 kinase)/protein kinase B (Akt), phospholipase C (PLC)-g/Ca2 and the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways. Phosphorylation of the docking protein, fibroblast growth factor receptor substrate 2 (FRS2) is followed by growth factor receptor-bound protein 2 (Grb2) activation, which in turns activates either the Ras/MAPK cascade via Son of Sevenless (SOS), or the PI-3 kinase/Akt pathway via Grb2-associated-binding protein 1 (Gab1). PI-3 kinase can also be activated directly by tyrosine phosphorylation or alternatively by Ras1. The other main transduction pathway involves PLC. The Src homology 2 (SH2) domain of the PLC interacts directly with the receptor leading to the hydrolysis of phosphatidyl-inositol-4,5-diphosphate (PIP2) to inositol-1,4,5-triphophate (IP-3) and diacylglycerol (DAG). Inositol-1,4,5-triphosphate (IP-3) releases Ca2+ from the endoplasmic reticulum (ER), while DAG activates protein kinase C (PKC) that in turn can activate the noncanonical planar cell polarity (PCP) pathway and RAF proto-oncogene serine/threonine-protein kinase (Raf1). Feedback inhibitors such as dual specificity phosphatase 6 (Dusp6)/mitogen-activated protein kinase phosphatase-3 (MKP-3), sprouty protein (Spry), FRS2a, sprouty-related, EVH1 domain-containing protein (Spred), and Sef involved in signal attenuation, and enhancers such as fibronectin leucine rich transmembrane protein 3 (XFLRT3) can also contribute to the overall levels of bFGF signaling. HSPGs, heparin sulphate proteoglycans; EMT, epithelial-to-mesenchymal transition; P, phosphorylation (modified from Villegas et al., 2010) [110] □ 2010 Wiley-Liss, Inc. with permission for reuse.

In vivo effects of basic fibroblast growth factor (bFGF)

Cell typesIn vivo resultsReferences
PDLSCs(–) bone formation in subcutaneous implantationLee et al., 2012 [93]
DPSCs(–) bone formation (1 week bFGF priming)Qian et al., 2014 [60]
(+) bone formation (2 week bFGF priming)(+) revascularization and cell migration in an ectopictooth slice transplantation modelYang et al., 2015 [113]
SHEDs(+) dentin-like structure formation in an ectopic transplantation modelsKim et al., 2014 [92]
(–) bone formation in ectopic transplantation modelsLi et al., 2012 [61]
Primary dental pulp cells from deciduous teeth(+) wound healing in a murine full-thickness skin defect modelNishino et al., 2011 [111]
(in vivo delivery without cell incorporation)(+) revascularization, recellularization, and odontoblastic differentiation in an ectopic tooth transplantation modelTakeuchi et al., 2015 [115]
Suzuki et al., 2011 [101]

In vitro effects of basic fibroblast growth factor (bFGF)

Cell typeIn vivo resultsReferences
DPSCs(+) cell migrationNishino et al., 2011 [111]
(+) cell proliferationMorito et al., 2009 [89]Lee et al., 2015 [112] He et al., 2008 [94]
(+) colony forming unitOsathanon et al., 2011 [9]
(+) matrix deposition and cell viabilityYang et al., 2015 [113]
(+) stem cell marker expression (STRO-1, Oct4, Nanog, Rex1)Morito et al., 2009 [89] Osathanon et al., 2011 [9]
(–) osteoblast differentiationQian J et al., 2014 [60] Morito et al., 2009 [89] Osathanon et al., 2011 [9]
(+) osteoblast differentiation (6 day or 2 weeks bFGF priming)Qian J et al., 2014 [60] Lee et al., 2015 [112]
(+) neurogenic differentiationSasaki et al., 2008 [114] Osathanon et al., 2011 [9]
PDLSCs(+) cell proliferationKono et al., 2013 [95] Lee et al., 2012 [93] Lee et al., 2015 [112] Takeuchi et al., 2015 [115]
(–) c-Kit expressionSuphanantachat et al., 2014 [116]
(–) osteoblast differentiationLee et al., 2012 [93] Osathanon et al., 2013 [11]
SHEDs(+) colony forming unitNowwarote et al., 2015 [98] Sukarawan et al., 2014 [10] Osathanon et al., 2013 [11] Kim et al., 2014 [92]
No influence on cell proliferationLi et al., 2012 [61] Sukarawan et al., 2014 [10]
(+) stem cell marker expression (Oct4, Nanog, Rex1)Sukarawan et al., 2014 [10]
(–) osteoblast differentiationNowwarote et al., 2015 [98] Osathanon et al., 2013 [11] Kim et al., 2014 [92] Li et al., 2012 [61]
(+) adipogenic and chondrogenic differentiationKim et al., 2014 [92]
SCAPs(+) cell proliferation and colony forming unit(+) stem cell marker expression (Oct4, Nanog, Rex1, Sox2,STRO-1)(–) osteoblast differentiationWu et al., 2012 [91]
Dental pulp cells(+) cell migrationTakeuchi et al., 2015 [115]
(+) cell proliferationTakeuchi et al., 2015 [115] Kim et al., 2010 [96]
(–) osteoblast differentiationTakeuchi et al., 2015 [115]
(+) odontoblast differentiationKim et al., 2010 [96]
Periodontal(+) cell migration and cell proliferationTakeuchi et al., 2015 [115]
ligament cellsKono et al., 2013[95]
(+) proliferation of STRO-1+/CD146+ cellsHidaka et al., 2012 [90]
(–) osteogenic differentiationDangaria et al., 2009 [117]
Dental follicle cells(–) osteogenic differentiationDangaria et al., 2009 [117]
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