scholarly journals The Effects of Platelet-Derived Growth Factor-BB on Bone Marrow Stromal Cell-Mediated Vascularized Bone Regeneration

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Maolin Zhang ◽  
Wenwen Yu ◽  
Kunimichi Niibe ◽  
Wenjie Zhang ◽  
Hiroshi Egusa ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Growth Factor ◽  
Bone Regeneration ◽  
Lentiviral Vector ◽  
Umbilical Vein ◽  
Adipogenic Differentiation ◽  
Platelet Derived Growth Factor ◽  
Extracellular Signal ◽  
Rat Calvarial Defect ◽  
Vascularized Bone

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.

Isolation and sequencing of a cDNA clone homologous to the v-sis oncogene from human endothelial cells

1986 ◽  
Vol 6 (8) ◽  
pp. 3018-3022
Author(s):  
B D Tong ◽  
S E Levine ◽  
M Jaye ◽  
G Ricca ◽  
W Drohan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Cdna Library ◽  
Cdna Clone ◽  
Umbilical Vein ◽  
Platelet Derived Growth Factor ◽  
Human Endothelial Cells ◽  
A Chain ◽  
Umbilical Vein Endothelial Cells ◽  
Reading Frames

A clone containing the 3' end of the mRNA for the human c-sis gene (homologous to the B chain of platelet-derived growth factor) was isolated from a cDNA library derived from human umbilical vein endothelial cells and then sequenced. The analysis of possible translation products in all three reading frames indicated that the A chain of platelet-derived growth factor was not coded for within the 3' end of the c-sis mRNA. The 3' end of the mRNA for c-sis is contained in or adjacent to exon 6.

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
Keyword(s):  
Growth Factor ◽  
Bone Regeneration ◽  
Bone Grafting ◽  
Bone Growth ◽  
Platelet Derived Growth Factor ◽  
Future Application ◽  
Second Phase ◽  
Bony Defect ◽  
Wound Site ◽  
Functioning Capillaries

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.

scholarly journals Platelet-derived growth factor does not stimulate prostacyclin synthesis by cultured endothelial cells

Blood ◽  
1986 ◽  
Vol 67 (1) ◽  
pp. 131-134
Author(s):  
KS Callahan ◽  
A Schorer ◽  
JM Harlan
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Umbilical Vein ◽  
Platelet Derived Growth Factor ◽  
Human Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Prostacyclin Synthesis ◽  
Release Product ◽  
Stimulation Of

We examined the effect of highly purified platelet-derived growth factor (PDGF) on prostacyclin (PGI2) release by cultured human umbilical vein and bovine aortic endothelial cells. PDGF tested at concentrations equal to or exceeding those observed in serum did not increase endothelial cell PGI2 synthesis as measured by radioimmunoassay of its metabolite, 6-keto-PGF1 alpha. In contrast, cells incubated with 20% human whole blood serum (WBS) demonstrated significantly increased PGI2 production (fivefold stimulation). Addition of anti-PDGF antibody to the 20% WBS did not attenuate the increased synthesis of PGI2. Incubation with 20% plasma-derived serum (PDS) that was deficient in PDGF produced stimulation of PGI2 release similar to 20% WBS. These results demonstrate that PDGF does not cause increased PGI2 synthesis in cultured human endothelial cells of human or bovine origin, and further suggest that the stimulation observed with serum is not due to a platelet-release product.

scholarly journals Direct recruitment of CRK and GRB2 to VEGFR-3 induces proliferation, migration, and survival of endothelial cells through the activation of ERK, AKT, and JNK pathways

Blood ◽  
2005 ◽  
Vol 106 (10) ◽  
pp. 3423-3431 ◽  
Author(s):  
Ahmad Salameh ◽  
Federico Galvagni ◽  
Monia Bardelli ◽  
Federico Bussolino ◽  
Salvatore Oliviero
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Umbilical Vein ◽  
Growth Factor Receptor ◽  
Mitogen Activated Protein Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Capillary Plexus ◽  
Primary Capillary Plexus ◽  
Umbilical Vein Endothelial Cells

AbstractVascular endothelial growth factor receptor-3 (VEGFR-3) plays a key role for the remodeling of the primary capillary plexus in the embryo and contributes to angiogenesis and lymphangiogenesis in the adult. However, VEGFR-3 signal transduction pathways remain to be elucidated. Here we investigated VEGFR-3 signaling in primary human umbilical vein endothelial cells (HUVECs) by the systematic mutation of the tyrosine residues potentially involved in VEGFR-3 signaling and identified the tyrosines critical for its function. Y1068 was shown to be essential for the kinase activity of the receptor. Y1063 signals the receptor-mediated survival by recruiting CRKI/II to the activated receptor, inducing a signaling cascade that, via mitogen-activated protein kinase kinase-4 (MKK4), activates c-Jun N-terminal kinase-1/2 (JNK1/2). Inhibition of JNK1/2 function either by specific peptide inhibitor JNKI1 or by RNA interference (RNAi) demonstrated that activation of JNK1/2 is required for a VEGFR-3–dependent prosurvival signaling. Y1230/Y1231 contributes, together with Y1337, to proliferation, migration, and survival of endothelial cells. Phospho-Y1230/Y1231 directly recruits growth factor receptor–bonus protein (GRB2) to the receptor, inducing the activation of both AKT and extracellular signal–related kinase 1/2 (ERK1/2) signaling. Finally, we observed that Y1063 and Y1230/Y1231 signaling converge to induce c-JUN expression, and RNAi experiments demonstrated that c-JUN is required for growth factor–induced prosurvival signaling in primary endothelial cells.

Shear stress increases endothelial platelet-derived growth factor mRNA levels

1991 ◽  
Vol 260 (2) ◽  
pp. H642-H646 ◽  
Author(s):  
H. J. Hsieh ◽  
N. Q. Li ◽  
J. A. Frangos
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Growth Factor ◽  
Umbilical Vein ◽  
Fold Increase ◽  
Platelet Derived Growth Factor ◽  
Mrna Levels ◽  
Cell Mitogen ◽  
Stress Dependent

We have investigated the effect of shear stress on platelet-derived growth factor (PDGF) A and B chain mRNA levels in cultured human umbilical vein endothelial cells (hUVEC). The levels of both PDGF A and B mRNA in hUVEC were increased by a physiological shear stress (16 dyn/cm2), reaching a maximum approximately 1.5-2 h after the onset of shear stress and returning almost to control values at 4 h. The peak levels showed a more than 10-fold enhancement for PDGF A mRNA and a 2- to 3-fold increase for PDGF B mRNA (P less than 0.05). PDGF A mRNA also showed a shear-dependent increase from 0 to 6 dyn/cm2 (P less than 0.05) and then plateaued from 6 to 51 dyn/cm2. PDGF B mRNA levels were elevated as shear stress increased from 0 to 6 dyn/cm2 then declined gradually to a minimum at 31 dyn/cm2 (P less than 0.05) and increased again when shear stress rose to 51 dyn/cm2 (P less than 0.05). PDGF, a potent smooth muscle cell mitogen and vasoconstrictor, released from the endothelium may regulate the blood flow in vivo. The shear stress-dependent elevation of PDGF A and B mRNA in endothelial cells may be involved in the adaptation of blood vessels to flow mediated by the endothelium.

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