Russell R Reid

The University of Chicago Medical Center, Chicago, Illinois, United States

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Publications (24)52.06 Total impact

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    ABSTRACT: The reconstructive goals for myelodysplastic defects are to provide a multilayered, tension-free and well-vascularized closure to prevent cerebrospinal fluid leakage, wound infection or breakdown and to optimize neurologic outcomes. We reviewed our ten-year experience with myelodysplastic defects and our preferred technique for large defects utilizing paraspinous flaps followed by V-Y crescentic rotation advancement flaps. A retrospective chart review was performed on all myelodysplastic defects closed at the University of Chicago Medicine from 2002 to 2012. Twenty-three patients were treated: eight were closed using V-Y crescentic rotation advancement flaps, eight primarily, two with transposition flaps and five with bilateral latissimus dorsi and gluteus maximus myocutaneous flaps. Patient defect characteristics, reconstructive details, follow up time, and wound complications were analyzed. The primary closure group included eight patients. There was one minor complication and two major complications that required debridement and plastic surgery consultation in this group. The transposition group included two patients and had no wound healing issues. The latissimus and gluteus myocutaneous group included five patients and had one minor wound healing issues. The V-Y crescentic group included eight patients. There were four minor wound breakdowns in the lateral donor sites and one major wound complication involving a CSF leak, meningitis and wound breakdown that required debridement. The groups were stratified by size, <5 cm and >5 cm, and further analyzed. Bilateral V-Y crescentic rotation advancement flap is a useful option when confronted with large myelodysplastic defects. It provides a multilayer, tension-free wound closure and spares the gluteus maximus and latissimus dorsi muscle groups.
    Journal of Plastic Reconstructive & Aesthetic Surgery 01/2014; · 1.44 Impact Factor
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    ABSTRACT: Composite cranial defects in the setting of infection, irradiation, or cerebrospinal fluid leak present a significant risk for devastating neurologic sequelae. Such defects require soft-tissue coverage and skeletal reconstruction that can withstand the hostile environment of a precarious wound. Patients with high-risk composite cranial defects treated with free flap reconstruction containing a vascularized osseous component from 2003 to 2012 were reviewed retrospectively. Fourteen patients received autologous vascularized cranioplasties between 2003 and 2012 with a mean age of 55.7 years and a mean follow-up of 14.1 months. Preoperatively, all patients had infection, irradiation, cerebrospinal fluid leak, or a combination thereof. Thirteen patients (92.9 percent) were reoperative cases for recurrent tumor, infection, or both. Six patients (42.9 percent) failed previous reconstructive procedures. Tissue biopsy-proven infection was present in 10 patients (71.4 percent) with calvarial osteomyelitis, both osteomyelitis and meningitis, or scalp soft-tissue infection only. Nine patients (64.3 percent) suffered from malignancy and six of these patients were irradiated preoperatively. Cranioplasty was achieved as part of a chimeric free flap using rib, scapula, both rib and scapula, or ilium. Vascularized duraplasty using serratus anterior fascia as a component of the chimeric flap was performed in three patients. No flap losses occurred and all patients had resolution of infection. Soft-tissue and skeletal restoration are the two critical components of composite cranial reconstruction. The authors report outcomes of the largest series of one-stage immediate cranioplasty consisting of autologous soft tissue and vascularized bone in high-risk composite cranial wounds and suggest its application in defects associated with compromised wound beds. Therapeutic, IV.
    Plastic and reconstructive surgery 10/2013; 132(4):967-75. · 2.74 Impact Factor
  • Jonathan Bank, Kelly J Ledbetter, Russell R Reid
    The Journal of craniofacial surgery 05/2013; 24(3):1054-1055. · 0.81 Impact Factor
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    ABSTRACT: The RUNX2 transcription factor regulates osteoblast differentiation. Its absence, as with cleidocranial dysplasia, results in deficient bone formation. However, its excess seems to follow a dose response of over ossification. RUNX2 duplications (3 copies) are exceedingly rare but have been reported to cause craniosynostosis. There are no existing reports of quadruplications (4 copies). We present a case study of a boy with an atypical skull deformity with pan-craniosynostosis whose microarray analysis revealed 4 copies of a 1.24-Mb region from 6p12.3 to 6p21.1 containing the RUNX2 gene. Further characterization of this osteogenic pathway may aid in our understanding of the pathogenesis and subsequent prevention and treatment of syndromic craniosynostosis.
    The Journal of craniofacial surgery 01/2013; 24(1):126-9. · 0.81 Impact Factor
  • Rina Patel, Russell R Reid, Colin S Poon
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    ABSTRACT: Maxillofacial fractures are very common. Recognizing patterns of facial fractures is helpful in assessing maxillofacial injury and accurately characterizing all fractures that may be present. Facial fractures are grouped into the following categories: nasal bone, naso-orbito-ethmoid, orbital, zygomatic, maxillary (including Le Fort-type fractures), mandibular, and frontal sinus fractures. Within each subgroup of facial fractures, there are key findings, whether of the fracture itself or of potential associated injuries, that are important factors in determining whether the patient is managed conservatively or with surgery. This article highlights the features of facial fractures that are the most important to the surgeons and provides a framework for effective radiological reporting.
    Seminars in ultrasound, CT, and MR. 10/2012; 33(5):410-7.
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    ABSTRACT: Craniofacial defect repair is often limited by a finite supply of available autologous tissue (ie, bone) and less than ideal alternatives. Therefore, other methods to produce bony healing must be explored. Several studies have demonstrated that low-frequency pulsed electromagnetic field (PEMF) stimulation (ie, 5-30 Hz) of osteoblasts enhances bone formation. The current study was designed to investigate whether a Food and Drug Administration-approved, high-frequency PEMF-emitting device is capable of inducing osteogenic differentiation of osteoprogenitor cells. Osteoprogenitor cells (commercially available C3H10T1/2 and mouse calvarial) in complete Dulbecco modified Eagle medium were continuously exposed to PEMF stimulation delivered by the ActiPatch at a frequency of 27.1 MHz. Markers of cellular proliferation and early, intermediate, and terminal osteogenic differentiation were measured and compared with unstimulated controls. All experiments were performed in triplicate. High-frequency PEMF stimulation increases alkaline phosphatase activity in both cell lines. In addition, high-frequency PEMF stimulation augments osteopontin and osteocalcin expression as well as mineral nodule formation in C3H10T1/2 cells, indicating late and terminal osteogenic differentiation, respectively. Cellular proliferation, however, was unaffected by high-frequency PEMF stimulation. Mechanistically, high-frequency PEMF-stimulated osteogenic differentiation is associated with elevated mRNA expression levels of osteogenic bone morphogenetic proteins in C3H10T1/2 cells. Our findings suggest that high-frequency PEMF stimulation of osteoprogenitor cells may be explored as an effective tissue engineering strategy to treat critical-size osseous defects of the craniofacial and axial skeleton. ABBREVIATIONS: ALP, alkaline phosphatase; BMP, bone morphogenetic protein; ERK-1, extracellular signal-regulated kinase 1; iCALs, immortalized calvarial cells; IHC, immunohistochemical; MAP, mitogen-activated protein; MSC, mesenchymal stem cell; OCN, osteocalcin; OPN, osteopontin; p38α, p38-reactivating kinase; PBS, phosphate-buffered saline; PEMF, pulsed electromagnetic field.
    The Journal of craniofacial surgery 03/2012; 23(2):586-93. · 0.81 Impact Factor
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    ABSTRACT: Critical-size osseous defects cannot heal without surgical intervention and can pose a significant challenge to craniofacial reconstruction. Autologous bone grafting is the gold standard for repair but is limited by a donor site morbidity and a potentially inadequate supply of autologous bone. Alternatives to autologous bone grafting include the use of alloplastic and allogenic materials, mesenchymal stem cells, and bone morphogenetic proteins. Bone morphogenetic proteins (BMPs) are essential mediators of bone formation involved in the regulation of differentiation of osteoprogenitor cells into osteoblasts. Here we focus on the use of BMPs in experimental models of craniofacial surgery and clinical applications of BMPs in the reconstruction of the cranial vault, palate, and mandible and suggest a model for the use of BMPs in personalized stem cell therapies.
    BioMed Research International 01/2012; 2012:601549. · 2.88 Impact Factor
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    ABSTRACT: Mesenchymal stem cells (MSCs) are multipotent cells which reside in many tissues and can give rise to multiple lineages including bone, cartilage and adipose. Although MSCs have attracted significant attention for basic and translational research, primary MSCs have limited life span in culture which hampers MSCs' broader applications. Here, we investigate if mouse mesenchymal progenitors can be conditionally immortalized with SV40 large T antigen and maintain long-term cell proliferation without compromising their multipotency. Using the system which expresses SV40 large T antigen flanked with Cre/loxP sites, we demonstrate that mouse embryonic fibroblasts (MEFs) can be efficiently immortalized by SV40 large T antigen. The conditionally immortalized MEFs (iMEFs) exhibit an enhanced proliferative activity and maintain long-term cell proliferation, which can be reversed by Cre recombinase. The iMEFs express most MSC markers and retain multipotency as they can differentiate into osteogenic, chondrogenic and adipogenic lineages under appropriate differentiation conditions in vitro and in vivo. The removal of SV40 large T reduces the differentiation potential of iMEFs possibly due to the decreased progenitor expansion. Furthermore, the iMEFs are apparently not tumorigenic when they are subcutaneously injected into athymic nude mice. Thus, the conditionally immortalized iMEFs not only maintain long-term cell proliferation but also retain the ability to differentiate into multiple lineages. Our results suggest that the reversible immortalization strategy using SV40 large T antigen may be an efficient and safe approach to establishing long-term cell culture of primary mesenchymal progenitors for basic and translational research, as well as for potential clinical applications.
    PLoS ONE 01/2012; 7(2):e32428. · 3.73 Impact Factor
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    ABSTRACT: Promoting osteogenic differentiation and efficacious bone regeneration have the potential to revolutionize the treatment of orthopaedic and musculoskeletal disorders. Mesenchymal Stem Cells (MSCs) are bone marrow progenitor cells that have the capacity to differentiate along osteogenic, chondrogenic, myogenic, and adipogenic lineages. Differentiation along these lineages is a tightly controlled process that is in part regulated by the Bone Morphogenetic Proteins (BMPs). BMPs 2 and 7 have been approved for clinical use because their osteoinductive properties act as an adjunctive treatment to surgeries where bone healing is compromised. BMP-9 is one of the least studied BMPs, and recent in vitro and in vivo studies have identified BMP-9 as a potent inducer of osteogenic differentiation in MSCs. BMP-9 exhibits significant molecular cross-talk with the Wnt/ β-catenin and other signaling pathways, and adenoviral expression of BMP-9 in MSCs increases the expression of osteogenic markers and induces trabecular bone and osteiod matrix formation. Furthermore, BMP-9 has been shown to act synergistically in bone formation with other signaling pathways, including Wnt/ β-catenin, IGF, and retinoid signaling pathways. These results suggest that BMP-9 should be explored as an effective bone regeneration agent, especially in combination with adjuvant therapies, for clinical applications such as large segmental bony defects, non-union fractures, and/or spinal fusions.
    Current Gene Therapy 04/2011; 11(3):229-40. · 5.32 Impact Factor
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    ABSTRACT: Craniosynostosis is a significant disorder affecting 1 in 2500 live births worldwide. Although a large body of work has focused on dural regulation and the contributions of molecular mediators such as fibroblast growth factor, bone morphogenetic protein, and transforming growth factor β, minimal attention has been directed toward osteoclast function in cranial suture biology. Receptor activator of nuclear factor κB (RANK) is an essential mediator of osteoclastogenesis and osteoclast activation. In this study, physiologic fusion of posterior frontal sutures in murine development correlated with decreasing protein expression of RANK in comparison to age-matched coronal and sagittal sutures via immunohistochemical survey. However, RANK mRNA did not exhibit a similar pattern suggesting that RANK is regulated at the protein level. Fused cranial sutures in nonsyndromic craniosynostotic children also showed decreased levels of RANK staining in immunohistochemistry in comparison to patent sutures from the same patients. Immunohistochemistry with a RANK ligand antibody did not show differences in fused or patent sutures. Moreover, RANK knockdown in calvarial strip suture cultures displayed increased bone density specifically in the suture line after infection with small interfering RANK viruses. Cranial suture biology, similar to bone biology in general, likely depends on a complex interplay between osteoblasts and osteoclasts. We now report a temporospatial correlation between RANK expression and suture morphology that suggests that osteoclast activity is important in maintenance of cranial suture patency in normal physiology and disease. Furthermore, RANK downregulation promoted suture fusion establishing a causal relationship between the presence of RANK and patency.
    The Journal of craniofacial surgery 03/2011; 22(2):699-705. · 0.81 Impact Factor
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    ABSTRACT: A mandibular arteriovenous malformation (AVM) presented with massive molar socket bleeding and was emergently treated by tooth extraction and partial resection of the surrounding alveolar bone. To achieve hemostasis, the resultant cavity was filled with hydroxyapatite bone cement. Not only was hemostasis and alveolar reconstruction achieved, but follow-up angiography demonstrated venous outlet occlusion and retrograde AVM thrombosis requiring no further treatment.
    Journal of neurointerventional surgery 03/2011; 3(1):92-4. · 1.38 Impact Factor
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    ABSTRACT: The Wnt pathway plays a critical role in development and differentiation of many tissues, such as the gut, hair follicles, and bone. Increasing evidence indicates that Wnts may function as key regulators in osteogenic differentiation of mesenchymal stem cells and bone formation. Conversely, aberrant Wnt signaling is associated with many osteogenic pathologies. For example, genetic alterations in the Wnt signaling pathway lead to osteoporosis and osteopenia, while inactivating mutations of Wnt inhibitors result in a hyperostotic skeleton with increased bone mineral density. Hyperparathyroidism causes osteopenia via induction of the Wnt signaling pathway. Lithium, often used to treat bipolar disorder, blocks a Wnt antagonist, decreasing the patient's risk of fractures. Thus, manipulating the Wnt pathway may offer plenty therapeutic opportunities in treating bone disorders. In fact, induction of the Wnt signaling pathway or inhibition of Wnt antagonists has shown promise in treating bone metabolic disorders, including osteoporosis. For example, antibodies targeting the Wnt inhibitor Sclerostin lead to increased bone mineral density in post-menopausal women. However, such therapies targeting the Wnt pathway are not without risk, as genetic alternations may lead to over-activation of Wnt/β-catenin and its association with many tumors. It is conceivable that targeting Wnt inhibitors may predispose the individuals to tumorigenic phenotypes, at least in bone. Here, we review the roles of Wnt signaling in bone metabolic and pathologic processes, as well as the therapeutic potential for targeting Wnt pathway and its associated risks in bone diseases.
    Current Molecular Pharmacology 01/2011; 4(1):14-25.
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    ABSTRACT: Stem cells are characterized by their capability to self-renew and terminally differentiate into multiple cell types. Somatic or adult stem cells have a finite self-renewal capacity and are lineage-restricted. The use of adult stem cells for therapeutic purposes has been a topic of recent interest given the ethical considerations associated with embryonic stem (ES) cells. Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into osteogenic, adipogenic, chondrogenic, or myogenic lineages. Owing to their ease of isolation and unique characteristics, MSCs have been widely regarded as potential candidates for tissue engineering and repair. While various signaling molecules important to MSC differentiation have been identified, our complete understanding of this process is lacking. Recent investigations focused on the role of epigenetic regulation in lineage-specific differentiation of MSCs have shown that unique patterns of DNA methylation and histone modifications play an important role in the induction of MSC differentiation toward specific lineages. Nevertheless, MSC epigenetic profiles reflect a more restricted differentiation potential as compared to ES cells. Here we review the effect of epigenetic modifications on MSC multipotency and differentiation, with a focus on osteogenic and adipogenic differentiation. We also highlight clinical applications of MSC epigenetics and nuclear reprogramming.
    Stem cells international. 01/2011; 2011:201371.
  • Lawrence J. Gottlieb, Russell R. Reid
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    ABSTRACT: In 1948, Sir Archibald McIndoe, when referring to reconstruction of the burned face, stated: “The aim is to produce a face which in sum is symmetrical in its separate parts, of good color and texture and freely mobile so that expression of mood is possible in all its infinite variety”. Three different cases are presented at varying levels of age and deformity. The techniques and plans designed to correct these deformities have been described in order to demonstrate the intense level of planning and technical understanding necessary for successful execution. We have demonstrated three different complex patients that have been treated successfully with current techniques. While not readily available for direct comparison, the level of deformity requires intense speculation and definitive treatment. While the debate regarding autologous versus interventional procedures will continue, these important issues deserve ongoing discussion in the light of informed debate.
    12/2010: pages 119-130;
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    ABSTRACT: Mesenchymal stem cells (MSCs) are non-hematopoietic stem cells with the capacity to differentiate into tissues of both mesenchymal and non-mesenchymal origin. MSCs can differentiate into osteoblastic, chondrogenic, and adipogenic lineages, although recent studies have demonstrated that MSCs are also able to differentiate into other lineages, including neuronal and cardiomyogenic lineages. Since their original isolation from the bone marrow, MSCs have been successfully harvested from many other tissues. Their ease of isolation and ex vivo expansion combined with their immunoprivileged nature has made these cells popular candidates for stem cell therapies. These cells have the potential to alter disease pathophysiology through many modalities including cytokine secretion, capacity to differentiate along various lineages, immune modulation and direct cell-cell interaction with diseased tissue. Here we first review basic features of MSC biology including MSC characteristics in culture, homing mechanisms, differentiation capabilities and immune modulation. We then highlight some in vivo and clinical evidence supporting the therapeutic roles of MSCs and their uses in orthopedic, autoimmune, and ischemic disorders.
    World journal of stem cells. 08/2010; 2(4):67-80.
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    ABSTRACT: An abstract is unavailable. This article is available as HTML full text and PDF.
    Plastic &amp Reconstructive Surgery 07/2010; 126(2):727. · 3.54 Impact Factor
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    ABSTRACT: Efficient osteogenic differentiation and bone formation from mesenchymal stem cells (MSCs) should have clinical applications in treating nonunion fracture healing. MSCs are adherent bone marrow stromal cells that can self-renew and differentiate into osteogenic, chondrogenic, adipogenic, and myogenic lineages. We have identified bone morphogenetic protein 9 (BMP-9) as one of the most osteogenic BMPs. Here we investigate the effect of insulin-like growth factor 2 (IGF-2) on BMP-9-induced bone formation. We have found that endogenous IGF-2 expression is low in MSCs. Expression of IGF-2 can potentiate BMP-9-induced early osteogenic marker alkaline phosphatase (ALP) activity and the expression of later markers. IGF-2 has been shown to augment BMP-9-induced ectopic bone formation in the stem cell implantation assay. In perinatal limb explant culture assay, IGF-2 enhances BMP-9-induced endochondral ossification, whereas IGF-2 itself can promote the expansion of the hypertropic chondrocyte zone of the cultured limb explants. Expression of the IGF antagonists IGFBP3 and IGFBP4 leads to inhibition of the IGF-2 effect on BMP-9-induced ALP activity and matrix mineralization. Mechanistically, IGF-2 is further shown to enhance the BMP-9-induced BMPR-Smad reporter activity and Smad1/5/8 nuclear translocation. PI3-kinase (PI3K) inhibitor LY294002 abolishes the IGF-2 potentiation effect on BMP-9-mediated osteogenic signaling and can directly inhibit BMP-9 activity. These results demonstrate that BMP-9 crosstalks with IGF-2 through PI3K/AKT signaling pathway during osteogenic differentiation of MSCs. Taken together, our findings suggest that a combination of BMP-9 and IGF-2 may be explored as an effective bone-regeneration agent to treat large segmental bony defects, nonunion fracture, and/or osteoporotic fracture.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 05/2010; 25(11):2447-59. · 6.04 Impact Factor
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    ABSTRACT: Mesenchymal progenitor cells (MPCs) are nonhematopoietic multipotent cells capable of differentiating into mesenchymal and nonmesenchymal lineages. While they can be isolated from various tissues, MPCs isolated from the bone marrow are best characterized. These cells represent a subset of bone marrow stromal cells (BMSCs) which, in addition to their differentiation potential, are critical in supporting proliferation and differentiation of hematopoietic cells. They are of clinical interest because they can be easily isolated from bone marrow aspirates and expanded in vitro with minimal donor site morbidity. The BMSCs are also capable of altering disease pathophysiology by secreting modulating factors in a paracrine manner. Thus, engineering such cells to maximize therapeutic potential has been the focus of cell/gene therapy to date. Here, we discuss the path towards the development of clinical trials utilizing BMSCs for orthopaedic applications. Specifically, we will review the use of BMSCs in repairing critical-sized defects, fracture nonunions, cartilage and tendon injuries, as well as in metabolic bone diseases and osteonecrosis. A review of www.ClinicalTrials.gov of the United States National Institute of Health was performed, and ongoing clinical trials will be discussed in addition to the sentinel preclinical studies that paved the way for human investigations.
    Stem cells international. 01/2010; 2010:519028.
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    ABSTRACT: Bone morphogenetic protein 9 (BMP-9) is a member of the transforming growth factor (TGF)-β/BMP superfamily, and we have demonstrated that it is one of the most potent BMPs to induce osteoblast differentiation of mesenchymal stem cells (MSCs). Here, we sought to investigate if canonical Wnt/β-catenin signalling plays an important role in BMP-9-induced osteogenic differentiation of MSCs. Wnt3A and BMP-9 enhanced each other’s ability to induce alkaline phosphatase (ALP) in MSCs and mouse embryonic fibroblasts (MEFs). Wnt antagonist FrzB was shown to inhibit BMP-9-induced ALP activity more effectively than Dkk1, whereas a secreted form of LPR-5 or low-density lipoprotein receptor-related protein (LRP)-6 exerted no inhibitory effect on BMP-9-induced ALP activity. β-Catenin knockdown in MSCs and MEFs diminished BMP-9-induced ALP activity, and led to a decrease in BMP-9-induced osteocalcin reporter activity and BMP-9-induced expression of late osteogenic markers. Furthermore, β-catenin knockdown or FrzB overexpression inhibited BMP-9-induced mineralization in vitro and ectopic bone formation in vivo, resulting in immature osteogenesis and the formation of chondrogenic matrix. Chromatin immunoprecipitation (ChIP) analysis indicated that BMP-9 induced recruitment of both Runx2 and β-catenin to the osteocalcin promoter. Thus, we have demonstrated that canonical Wnt signalling, possibly through interactions between β-catenin and Runx2, plays an important role in BMP-9-induced osteogenic differentiation of MSCs.
    Journal of Cellular and Molecular Medicine 07/2009; 13(8b):2448 - 2464. · 4.75 Impact Factor
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    ABSTRACT: Pluripotent mesenchymal stem cells (MSCs) are bone marrow stromal progenitor cells that can differentiate into osteogenic, chondrogenic, adipogenic, and myogenic lineages. We previously demonstrated that bone morphogenetic protein (BMP) 9 is one of the most potent and yet least characterized BMPs that are able to induce osteogenic differentiation of MSCs both in vitro and in vivo. Here, we conducted gene expression-profiling analysis and identified that Hey1 of the hairy/Enhancer of split-related repressor protein basic helix-loop-helix family was among the most significantly up-regulated early targets in BMP9-stimulated MSCs. We demonstrated that Hey1 expression was up-regulated at the immediate early stage of BMP9-induced osteogenic differentiation. Chromatin immunoprecipitation analysis indicated that Hey1 may be a direct target of the BMP9-induced Smad signaling pathway. Silencing Hey1 expression diminished BMP9-induced osteogenic differentiation both in vitro and in vivo and led to chondrogenic differentiation. Likewise, constitutive Hey1 expression augmented BMP9-mediated bone matrix mineralization. Hey1 and Runx2 were shown to act synergistically in BMP9-induced osteogenic differentiation, and Runx2 expression significantly decreased in the absence of Hey1, suggesting that Runx2 may function downstream of Hey1. Accordingly, the defective osteogenic differentiation caused by Hey1 knockdown was rescued by exogenous Runx2 expression. Thus, our findings suggest that Hey1, through its interplay with Runx2, may play an important role in regulating BMP9-induced osteoblast lineage differentiation of MSCs.
    Journal of Biological Chemistry 12/2008; 284(1):649-59. · 4.65 Impact Factor

Publication Stats

361 Citations
166 Downloads
2k Views
52.06 Total Impact Points

Institutions

  • 2007–2014
    • The University of Chicago Medical Center
      • • Section of Plastic and Reconstructive Surgery
      • • Department of Surgery
      Chicago, Illinois, United States
  • 2012
    • Chongqing University
      • School of Bioengineering
      Chongqing, Chongqing Shi, China
  • 2008
    • University of Chicago
      • Department of Surgery
      Chicago, Illinois, United States
    • Chongqing Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China