A New Protein Expressed in Bone Marrow Cells and Osteoblasts with Implication in Osteoblast Recruitment

Wurtz, Tilmann; Krüger, Anders; Christersson, Cecilia; Lundmark, Carin

doi:10.1006/excr.2000.5114

Cited by 29 publications

(38 citation statements)

References 19 publications

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“…RP59 has been identified in bone marrow cells with the capacity to differentiate into osteoblasts [46]. We further used antibodies against RP59 to identify the mesenchymal stem cells during bone formation in the segmental defect.…”

Section: Rp59 Expression and Cell Morphologymentioning

confidence: 99%

Recruitment of mesenchymal stem cells and expression of TGF-$beta;1 and VEGF in the early stage of shock wave-promoted bone regeneration of segmental defect in rats

CHEN¹

2004

Journal of Orthopaedic Research

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Extracorporeal shock wave (ESW) treatment has recently been established as a method to enhance bone repair. Here, we reported that ESW-promoted healing of segmental defect via stimulation of mesenchymal stem cell recruitment and differentiation into bone forming cells. Rats with a segmental femoral defect were exposed to a single ESW treatment (0.16 mJ/mm?, 1 Hz, 500 impulses). Cell morphology and histological changes in the defect region were assessed 3, 7, 14, and 28 days post-treatment. Presence of mesenchymal stem cell was assayed by immuno-staing for RPS9, a recently discovered marker, and also production of TGF-PI and VEGF was monitored. ESW treatment increased total cell density and the proportion of RP59 positive cells in the defect region. High numbers of round-and cuboidal-shaped cells strongly expressing RPS9 were initially found. Later, the predominant cell type was spindle-shaped fibroblastic cells, subsequently, aggregates of osteogenic and chondrogenic cells were observed. Histological observation suggested that bone marrow stem cells were progressively differentiated into osteoblasts and chondrocytes. RP59 staining was initially intense and decreased with the appearance of expression depended on the differentiation states of osteogenic and chondrogenic cells during the regeneration phase. Mature chondrocytes and osteoblasts exhibited only slight RP59 immunoreactivity. Expression of TGF-PI and VEGF-A mRNA in the defect tissues was also significantly increased ( P < 0.05) after ESW treatment as determined by RT-PCR. Intensive TGF-PI immuno-reactivity was induced immediately, whereas a lag period was observed for VEGF-A. Chondrocytes and osteoblasts at the junction of ossified cartilage clearly exhibited VEGF-A expression. Our findings suggest that recruitment of meseoblasts at the junction of ossified cartilage clearly exhibited mesenchymal stem cells is a critical step in bone reparation that is enhanced by ESW treatment. TGF-P1 and VEGF-A are proposed to play a chemotactic and mitogenic role in recruitment and differentiation of mesenchymal stem cells.

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Section: Rp59 Expression and Cell Morphologymentioning

confidence: 99%

Recruitment of mesenchymal stem cells and expression of TGF-$beta;1 and VEGF in the early stage of shock wave-promoted bone regeneration of segmental defect in rats

CHEN¹

2004

Journal of Orthopaedic Research

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“…Erythroid differentiation-associated gene (EDAG), which is homologous to mouse hemogen 1 and rat RP59, 2 is identified by using the polymerase chain reaction (PCR)-based subtractive hybridization method. 3 In a previous study, Yang et al 1 found that hemogen transcripts are specifically detected in blood islands, primitive blood cells and fetal liver and downregulated in the process of blood cell differentiation during mouse embryogenesis, then remain in the bone marrow and spleen in adult mice.…”

Section: Introductionmentioning

confidence: 99%

EDAG regulates the proliferation and differentiation of hematopoietic cells and resists cell apoptosis through the activation of nuclear factor-κB

Yao

et al. 2004

Cell Death Differ

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Erythroid differentiation-associated gene (EDAG) is considered to be a human hematopoiesis-specific gene. Here, we reported that downregulation of EDAG protein in K562 cells resulted in inhibition of growth and colony formation, and enhancement of sensitivity to erythroid differentiation induced by hemin. Overexpression of EDAG in HL-60 cells significantly blocked the expression of the monocyte/ macrophage differentiation marker CD11b after pentahydroxytiglia myristate acetate induction. Moreover, overexpression of EDAG in pro-B Ba/F3 cells prolonged survival and increased the expression of c-Myc, Bcl-2 and Bcl-xL in the absence of interleukin-3 (IL-3). Furthermore, we showed that EDAG enhanced the transcriptional activity of nuclear factorkappa B (NF-jB), and high DNA-binding activity of NF-jB was sustained in Ba/F3 EDAG cells after IL-3 was withdrawn. Inhibition of NF-jB activity resulted in promoting Ba/F3 EDAG cells death. These results suggest that EDAG regulates the proliferation and differentiation of hematopoietic cells and resists cell apoptosis through the activation of NF-jB.

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“…HEMGN was originally characterized as a hematopoietic gene with expression restricted to the hematopoietic system (Lu et al, 2001;Wurtz et al, 2001;Yang et al, 2001;Kruger et al, 2002). During embryogenesis, spatiotemporal expression patterns of HEMGN mark the ontogeny of hematopoiesis.…”

Section: Introductionmentioning

confidence: 99%

“…In hematopoietic cells, HEMGN is primarily expressed in erythroid and megakaryocytic lineages and is absent in lymphoid lineage and granulocytes (Yang et al, 2001;Kruger et al, 2002). In addition to expression in hematopoietic cells, HEMGN is also detected in osteoblasts (Wurtz et al, 2001) and in the primitive ectoderm and primitive streak (Kruger et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Sequence analysis reveals several protein motifs, including a nuclear localization signal and an array of 14-mer repeats with phased phosphorylation sites (Yang et al, 2001;Wurtz et al, 2001;Kruger et al, 2002). Functionally, Hemogen is likely to be an oncogene, because overexpression of human HEMGN in NIH 3T3 cells causes cell transformation and tumor formation in nude mice (Lu et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Alternative promoters and polyadenylation regulate tissue‐specific expression of Hemogen isoforms during hematopoiesis and spermatogenesis

Yang

Heng

Wan

et al. 2003

Developmental Dynamics

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Hemogen is a nuclear protein encoded by HEMGN (also known as hemogen in mouse, EDAG in human and RP59 in rat). It is considered to be a hematopoiesis-specific gene that is expressed during the ontogeny of hematopoiesis. Herein, we characterize two distinct splicing variants of HEMGN mRNA with restricted expression to hematopoietic cells and to round spermatids in the testis, respectively. Expression of the testis-specific HEMGN mRNA (HEMGN-t) is developmentally regulated and is concurrent with the first wave of meiosis in prepuberal mice. Sequence analysis reveals that HEMGN-t and the hematopoietic HEMGN mRNA (HEMGN-h) share a common coding sequence with distinct 5 and 3 untranslated regions and that these two isoforms are transcribed from the same gene locus, HEMGN, through the use of alternative promoters and polyadenylation sites. Thus, HEMGN expression exemplifies a developmental regulatory mechanism by which the diversification of gene expression is achieved through using distinct regulatory sequences in different cell types. Moreover, the existence of a testis-specific isoform of HEMGN suggests a role in spermatogenesis. Finally, fluorescence in situ hybridization demonstrates that HEMGN is localized to chromosome 4 A5-B2 in mouse and to chromosome 9q22 in human, which is a region known to harbor a cluster of leukemia breakpoints. Developmental Dynamics 228:606 -616, 2003.

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A New Protein Expressed in Bone Marrow Cells and Osteoblasts with Implication in Osteoblast Recruitment

Cited by 29 publications

References 19 publications

Recruitment of mesenchymal stem cells and expression of TGF-$beta;1 and VEGF in the early stage of shock wave-promoted bone regeneration of segmental defect in rats

Recruitment of mesenchymal stem cells and expression of TGF-$beta;1 and VEGF in the early stage of shock wave-promoted bone regeneration of segmental defect in rats

EDAG regulates the proliferation and differentiation of hematopoietic cells and resists cell apoptosis through the activation of nuclear factor-κB

Alternative promoters and polyadenylation regulate tissue‐specific expression of Hemogen isoforms during hematopoiesis and spermatogenesis

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