Effects of Pleiotrophin (PTN) Over-expression on Mouse Long Bone Development, Fracture Healing and Bone repair

  title={Effects of Pleiotrophin (PTN) Over-expression on Mouse Long Bone Development, Fracture Healing and Bone repair},
  author={G. Li and Jonathan R Bunn and Moses Mushipe and Q. He and X. Chen},
  journal={Calcified Tissue International},
Pleiotrophin (PTN) was found to have potent effects on regulation of osteoblast recruitment, proliferation and differentiation. The present study examined the long-term effects of targeted PTN over-expression on bone development and repair in a transgenic mouse model. Femurs and tibiae from the PTN transgenic mice and the wild type mice at age 1, 2, 4, 6, 12 and 24 months were collected, and examined by radiography, peripheral quantitative computed tomography (pQCT), histology and mechanical… 
Effects of Pleiotrophin Overexpression on Mouse Skeletal Muscles in Normal Loading and in Actual and Simulated Microgravity
Although little benefit was found in HU muscle disuse, PTN may emerge useful in various muscle diseases, because it exerts synergetic actions on muscle fibers and vessels, which could enforce oxidative metabolism and ameliorate muscle performance.
Pleiotropin enhances the osteo/dentinogenic differentiation potential of dental pulp stem cells
It is demonstrated that PTN has a positive role in maintaining DPSCs proliferation and osteo/dentinogenic differentiation potential and proliferation ability caused by PTN depletion.
Global Age-Dependent Differences in Gene Expression in Response to Calvarial Injury
Comparison of genomewide expression patterns during active regeneration after injury with calvaria in skeletally immature and mature mice suggests the importance of balanced osteoclast-mediated bone resorption for ultimate healing and highlights the potential role of retinoic acid signaling and the prostaglandin axis on skeletal regeneration.
The systemic angiogenic response during bone healing
Fracture healing in human subjects is accompanied by distinct changes in systemic levels of specific angiogenic factors, and significant alterations of these physiologic changes in patients developing a fracture nonunion over time could be detected as early as 2 weeks after initial trauma surgery.
Estrogen Stimulation of Pleiotrophin Enhances Osteoblast Differentiation and Maintains Bone Mass in IGFBP-2 Null Mice.
It is concluded that loss of IGFBP-2 expression is accompanied by upregulation of PTN and RPTPβ expression in osteoblasts, that the degree of increase is greater in females due to estrogen secretion, and that this compensatory change may account for some component of the maintenance of normal bone mass in female mice.
Regulation of Angiogenesis Discriminates Tissue Resident MSCs from Effective and Defective Osteogenic Environments †
In vitro, non-union site derived MSCs have no impairment of differentiation capacity, but they differ from IP-derived M SCs in mediating angiogenesis, and may be strongly implicated in the formation of the immature vascular network at the non- union site.
Differential Gene Expression between Juvenile and Adult Dura Mater: A Window into What Genes Play a Role in the Regeneration of Membranous Bone
A more differentiated osteoprogenitor population to exist along with a greater presence of osteoclasts in the juvenile dura mater relative to adults is suggested.
Spaceflight Influences both Mucosal and Peripheral Cytokine Production in PTN-Tg and Wild Type Mice
Spaceflight is associated with several health issues including diminished immune efficiency. Effects of long-term spaceflight on selected immune parameters of wild type (Wt) and transgenic mice


Effects of targeted overexpression of pleiotrophin on postnatal bone development.
Pleiotrophin/Osteoblast‐Stimulating Factor 1: Dissecting Its Diverse Functions in Bone Formation
It is proposed that PTN is an accessory signaling molecule, which is involved in a variety of processes in bone formation, and enhances or inhibits primary responses depending on the prevailing concentrations, the primary stimulus, and the availability of appropriate receptors.
Induction of Human Osteoprogenitor Chemotaxis, Proliferation, Differentiation, and Bone Formation by Osteoblast Stimulating Factor‐1/Pleiotrophin: Osteoconductive Biomimetic Scaffolds for Tissue Engineering
  • Xuebin B. Yang, R. Tare, R. Oreffo
  • Biology
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2003
PTN has the ability to promote adhesion, migration, expansion, and differentiation of human osteoprogenitor cells, and these results indicate the potential to develop protocols for de novo bone formation for skeletal repair that exploit cell‐matrix interactions.
Bone mass loss due to estrogen deficiency is compensated in transgenic mice overexpressing human osteoblast stimulating factor-1.
In ovariectomized mice, bone mass loss due to estrogen deficiency was observed in both transgenic and control mice but bone mass was still higher in transgenic mice than in controls, suggesting a new way to treat osteoporosis with OSF-1.
Cell Proliferation and Apoptosis During Fracture Healing
It is indicated that cell proliferation and apoptosis are coupled events during fracture repair, cell proliferation is active at the early stages, and apoptotic activity is active during the phase of callus remodeling.
Osteoblast Recruitment and Bone Formation Enhanced by Cell Matrix–associated Heparin-binding Growth-associated Molecule (HB-GAM)
It is shown here that heparin-binding growth-associated molecule (HB-GAM), an extracellular matrix–associated protein that enhances migratory responses in neurons, is prominently expressed in the cell matrices that act as target substrates for bone formation.
Heparin-binding proteins HB-GAM (pleiotrophin) and amphoterin in the regulation of cell motility.
A reliable externally fixated murine femoral fracture model that accounts for variation in movement between animals
Pleiotrophin: a cytokine with diverse functions and a novel signaling pathway.
Pleiotrophin is the first ligand of any of the known transmembrane tyrosine phosphatases and regulates both normal cell functions and different pathological conditions at many levels.