A Review of Platelet Derived Growth Factor Playing Pivotal Role in Bone Regeneration

2014 ◽  
Vol 40 (3) ◽  
pp. 330-340 ◽  
Author(s):  
Prasun Shah ◽  
Louise Keppler ◽  
James Rutkowski

This article is focused on the literature review and study of recent advances in the field of bone grafting, which involves platelet-derived growth factor (PDGF) as one of the facilitating factors in bone regeneration. This article includes a description of the mechanism of PDGF for use in surgeries where bone grafting is required, which promotes future application of PDGF for faster bone regeneration or inhibition of bone growth if required as in osteosarcoma. The important specific activities of PDGF include mitogenesis (increase in the cell populations of healing cells), angiogenesis (endothelial mitoses into functioning capillaries), and macrophage activation (debridement of the wound site and a second phase source of growth factors for continued repair and bone regeneration). Thus PDGF can be utilized in wound with bone defect to conceal the wound with repair of bony defect.

2001 ◽  
Vol 31 (1) ◽  
pp. 1
Author(s):  
Seung-Yeol Lee ◽  
Yang-Jo Seol ◽  
Yong-Moo Lee ◽  
Ju-Yeon Lee ◽  
Seung-Jin Lee ◽  
...  

2012 ◽  
Vol 23 (8) ◽  
pp. 1903-1912 ◽  
Author(s):  
J. J. Delgado ◽  
Esther Sánchez ◽  
Manuel Baro ◽  
Ricardo Reyes ◽  
Carmen Évora ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Maolin Zhang ◽  
Wenwen Yu ◽  
Kunimichi Niibe ◽  
Wenjie Zhang ◽  
Hiroshi Egusa ◽  
...  

Regenerative medicine for bone tissue mainly depends on efficient recruitment of endogenous or transplanted stem cells to guide bone regeneration. Platelet-derived growth factor (PDGF) is a functional factor that has been widely used in tissue regeneration and repair. However, the short half-life of PDGF limits its efficacy, and the mechanism by which PDGF regulates stem cell-based bone regeneration still needs to be elucidated. In this study, we established genetically modified PDGF-B-overexpressing bone marrow stromal cells (BMSCs) using a lentiviral vector and then explored the mechanism by which PDGF-BB regulates BMSC-based vascularized bone regeneration. Our results demonstrated that PDGF-BB increased osteogenic differentiation but inhibited adipogenic differentiation of BMSCs via the extracellular signal-related kinase 1/2 (ERK1/2) signaling pathway. In addition, secreted PDGF-BB significantly enhanced human umbilical vein endothelial cell (HUVEC) migration and angiogenesis via the phosphatidylinositol 3 kinase (PI3K)/AKT and ERK1/2 signaling pathways. We evaluated the effect of PDGF-B-modified BMSCs on bone regeneration using a critical-sized rat calvarial defect model. Radiography, micro-CT, and histological analyses revealed that PDGF-BB overexpression improved BMSC-mediated angiogenesis and osteogenesis during bone regeneration. These results suggest that PDGF-BB facilitates BMSC-based bone regeneration by enhancing the osteogenic and angiogenic abilities of BMSCs.


1991 ◽  
Vol 279 (2) ◽  
pp. 559-565 ◽  
Author(s):  
R Plevin ◽  
S J Cook ◽  
S Palmer ◽  
M J O Wakelam

Platelet-derived growth factor (PDGF) stimulated sn-1,2-diacylglycerol (DAG) mass formation in Swiss 3T3 fibroblasts with a lag time of some 30 s. The response was biphasic, with the second phase being sustained over time. PDGF also stimulated the formation of Ins(1,4,5)P3 with a similar lag time to the DAG response, suggesting that DAG is derived from PtdIns(4,5)P2 hydrolysis at this time point. PDGF-stimulated phosphatidylcholine (PtdCho) hydrolysis in Swiss 3T3 fibroblasts, as measured by the formation of water-soluble choline metabolites and phosphatidylbutanol (PtdBut) accumulation, was by a phospholipase D (PLD)-catalysed pathway which was kinetically downstream of initial PtdIns(4,5)P2 hydrolysis. Accumulation of PtdBut increased up to 15 min, suggesting that PLD activity is not rapidly densitized in response to PDGF. The kinetics of PtdCho hydrolysis closely paralleled the second phase of DAG formation, strongly suggesting that during prolonged stimulation periods PtdCho is a major source of DAG in these cells. However, since PtdIns(4,5)P2 breakdown was also prolonged, PDGF-stimulated DAG may be derived from both phospholipids. Down-regulation of protein kinase C (PKC), by pre-treatment with phorbol 12-myristate 13-acetate, abolished both [3H]choline and [3H]PtdBut formation, suggesting that PLD-catalysed PtdCho hydrolysis may be dependent on PKC activation, supporting its dependence on prior PtdIns(4,5)P2 hydrolysis.


Sign in / Sign up

Export Citation Format

Share Document