Systemically transplanted bone marrow stromal cells contributing to bone tissue regeneration

Li, Shuang; Tu, Qisheng; Zhang, J.; Stein, Gary S.; Lian, Jane B.; Yang, Pishan; Chen, Jake Y.

doi:10.1002/jcp.21302

Cited by 31 publications

(28 citation statements)

References 29 publications

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“…Briefly, bone donors were 3-day-old mBSP9.0Luc/␤-ACT-EGFP transgenic mice double-labeled with EGFP driven by ␤-actin promoter and luciferase driven by bone sialoprotein (BSP) promoter (37). After euthanasia, femurs from both sides of the donor mice were isolated and explanted into the back muscles of 8 -10-week-old wild type or adiponectin knock-out mice (stock no.…”

Section: Methodsmentioning

confidence: 99%

“…One femur was transplanted into an adiponectin knock-out mouse and the other into a wild type (WT) mouse; the mice were littermates generated by crossing a pair of heterozygous adiponectinϩϪ mice. At weeks 2 and 4 postoperatively, luciferase and EGFP expressions were measured using an IVIS Imaging System 200 Series in the live animals (Xenogen Corp., Alameda, CA) as described previously (37,38). Four weeks after explantation, the bone explants were harvested to measure bone length and ash/dry weight (39).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Adiponectin Inhibits Osteoclastogenesis and Bone Resorption via APPL1-mediated Suppression of Akt1

Jin

Dong³

et al. 2011

Journal of Biological Chemistry

100

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Adiponectin is an adipokine playing an important role in regulating energy homeostasis and insulin sensitivity. However, the effect of adiponectin on bone metabolism shows contradictory results according to different research studies. In this study femurs were isolated from genetically doublelabeled mBSP9.0Luc/␤-ACT-EGFP transgenic mice and were transplanted into adiponectin knock-out mice or wild type mice to investigate the effect of temporary exposure to adiponectin deficiency on bone growth and metabolism. We found that the growth of bone explants in adiponectin knock-out mice was significantly retarded. Histological analysis, microcomputed tomography analysis, and tartrate-resistant acid phosphatase staining revealed reduced trabecular bone volume, decreased cortical bone, and increased osteoclast number in bone explants in adiponectin knock-out mice. We then found that adiponectin inhibits RANKL-induced osteoclastogenesis from RAW264.7 cells and down-regulates RANKL-enhanced expressions of osteoclastogenic regulators including NFAT2, TRAF6, cathepsin K, and tartrate-resistant acid phosphatase. Adiponectin also increases osteoclast apoptosis and decreases survival/proliferation of osteoclast precursor cells. Using siRNA specifically targeting APPL1, the first identified adaptor protein of adiponectin signaling, we found that the inhibitory effect of adiponectin on osteoclasts was induced by APPL1-mediated down-regulation of Akt1 activity. In addition, overexpression of Akt1 successfully reversed adiponectin-induced inhibition in RANKL-stimulated osteoclast differentiation. In conclusion, adiponectin is important in maintaining the balance of energy metabolism, inflammatory responses, and bone formation.Adipose tissue is not just an inert organ for energy storage. It also secretes proinflammatory cytokines and synthesizes a wide range of biologically active molecules known as adipokines (1, 2). Adiponectin, a 30-kDa protein containing a collagen-repeat domain at the N terminus and a globular domain at the C terminus, is among these adipokines (3). It has been reported that adiponectin plays an important role in regulating energy homeostasis and insulin sensitivity, and plasma adiponectin levels correlate positively with insulin sensitivity (4, 5). APPL1 (adaptor protein containing pleckstrin homology domain, phosphotyrosine domain, and leucine zipper motif), is the first identified protein interacting with adiponectin receptors and is suggested to be an adaptor protein responsible for the mediation of adiponectin signal transduction (6). Knockdown of APPL1 expression resulted in a significant reduction in insulin-stimulated Akt phosphorylation (6). In addition to its insulin-sensitizing effect, adiponectin has also been reported to have potent antiinflammatory properties by suppressing the expressions of inflammatory cytokines while inducing production of anti-inflammatory cytokines (7-9). However, unlike other adipose tissue-derived molecules, adiponectin mRNA and plasma protein levels were shown to decreas...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Adiponectin Inhibits Osteoclastogenesis and Bone Resorption via APPL1-mediated Suppression of Akt1

Jin

Dong³

et al. 2011

Journal of Biological Chemistry

100

View full text Add to dashboard Cite

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“…Bone marrow-derived cells (BMDCs) are capable of homing to many tissues in response to injury signals and differentiating into tissue-specific cells, including muscle, liver, brain, pancreases islet, and even epithelial lineages, suggesting high developmental plasticity (Lagasse et al, 2000;Krause et al, 2001;Badiavas et al, 2003;Hess et al, 2003;Mezey et al, 2003;Li et al, 2008). However, the potential of the BMDCs to contribute to the dental mesenchymal cells is still unknown.…”

mentioning

confidence: 98%

Role of bone marrow‐derived progenitor cells in the maintenance and regeneration of dental mesenchymal tissues

Zhou

Shi

et al. 2011

Journal Cellular Physiology

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While dental mesenchymal stem cells are well-studied, the origin of these cells is still unclear. Bone marrow-derived cells (BMDCs) have the potential to engraft into several tissues after injury, but whether they can become dental tissue-specific progenitor cells under normal conditions and the relationship of these cells to the tissue-resident cells are unknown. Thus, we transplanted green fluorescent protein (GFP)-labeled BMDCs into irradiated wild-type mice. We found that the engraftment of BMDCs participated in the regeneration and differentiated into periodontal specific cells after injury. Under normal conditions, there were more BMDCs engrafting into the dental mesenchymal tissue than other organs, in which the expression of stromal cell-derived factor-1 (SDF-1) was significantly higher than in other organs, and the engraftment of cells increased with time. A small fraction of GFP+ cells maintained the mesenchymal stem cell phenotype positive for CD105, CD106, and CD90, which were significantly less than the tissue-resident stem cells; meanwhile, GFP+/CD45+ cells were rare. Isolation and characterization of the dental pulp cells showed that the number of GFP+/Ki67+ cells were greater than the GFP-/Ki67+ cells. In addition, some GFP+ cells differentiated into the dental-specific cells and expressed dental-specific proteins, and can be found in the odontoblast layer after implantation of the apical bud. In conclusion, these data suggest that bone marrow progenitor cells communicate with dental tissues and become tissue-specific mesenchymal progenitor cells to maintain tissue homeostasis.

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“…BSP-Luc/ACTB-EGFP mice were genetically double labelled with a luciferase reporter gene driven by a bone sialoprotein (BSP) promoter and an enhanced green fluorescent protein (EGFP) driven by a beta-actin promoter (Li et al, 2008). The BMSCs were obtained and cultured as described previously (Wu et al, 2003;Valverde et al, 2005).…”

Section: Bmsc Culture and Gene Transductionmentioning

confidence: 99%

“…BMSCs are capable of selfrenewal and can differentiate into several phenotypes including osteoblasts, chondroblasts, and adipocytes (Nussenbaum and Krebsbach, 2006;Robey and Bianco, 2006). Osteoblast progenitors are recruited from bone marrow and are involved in bone regeneration from peripheral circulation (Li et al, 2008). Transplanted BMSCs can be recruited from peripheral circulation to implantation sites and participate in the osseointegration of the titanium implants (Xu et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Transcription factor and bone marrow stromal cells in osseointegration of dental implants

Yan

Zhang

et al. 2013

eCM

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Titanium implants are widely used in dental clinics and orthopaedic surgery. However, bone formation surrounding the implant is relatively slow after inserting the implant. The current study assessed the effects of bone marrow stromal cells (BMSCs) with forced expression of special AT-rich sequence-binding protein 2 (SATB2) on the osseointegration of titanium implants. To determine whether SATB2 overexpression in BMSCs can enhance the osseointegration of implants, BMSCs were infected with the retrovirus encoding Satb2 (pBABE-Satb2) and were locally applied to bone defects before implanting the titanium implants in the mouse femur. Seven and twentyone days after implantation, the femora were isolated for immunohistochemical (IHC) staining, haematoxylin eosin (H&E) staining, real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), and micro-computed tomography (μCT) analysis. IHC staining analysis revealed that SATB2-overexpressing BMSCs were intensely distributed in the bone tissue surrounding the implant. Histological analysis showed that SATB2-overexpressing BMSCs significantly enhanced new bone formation and bone-to-implant contact 3 weeks after implantation. Real-time qRT-PCR results showed that the local delivery of SATB2-overexpressing BMSCs enhanced expression levels of potent osteogenic transcription factors and bone matrix proteins in the implantation sites. μCT analysis demonstrated that SATB2-overexpressing BMSCs significantly increased the density of the newly formed bone surrounding the implant 3 weeks postoperatively. These results conclude that local delivery of SATB2-overexpressing BMSCs significantly accelerates osseointegration of titanium implants. These results provide support for future pharmacological and clinical applications of SATB2, which accelerates bone regeneration around titanium implants.

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Systemically transplanted bone marrow stromal cells contributing to bone tissue regeneration

Cited by 31 publications

References 29 publications

Adiponectin Inhibits Osteoclastogenesis and Bone Resorption via APPL1-mediated Suppression of Akt1

Adiponectin Inhibits Osteoclastogenesis and Bone Resorption via APPL1-mediated Suppression of Akt1

Role of bone marrow‐derived progenitor cells in the maintenance and regeneration of dental mesenchymal tissues

Transcription factor and bone marrow stromal cells in osseointegration of dental implants

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