Importance of Membrane- or Matrix-Associated Forms of M-CSF and RANKL/ODF in Osteoclastogenesis Supported by SaOS-4/3 Cells Expressing Recombinant PTH/PTHrP Receptors

Itoh, Kanami; Udagawa, Nobuyuki; Matsuzaki, Kei; Miki, Takami; Amano, Hitoshi; Shinki, Toshimasa; Ueno, Yutaka; Takahashi, Naoyuki; Suda, Toshio

doi:10.1359/jbmr.2000.15.9.1766

Cited by 84 publications

(57 citation statements)

References 39 publications

(79 reference statements)

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“…22,27,67 In vitro experiments have shown that it is biologically active as an extracted membrane protein 28 and that it is active in situ for macrophage proliferation, 25,[68][69][70] for myelopoiesis, 38,69 and for osteoclastogenesis. 29,39,40 Recently, a csCSF-1 transgene driven by the collagen I␣ promoter has been shown to correct the bone density and tooth eruption defects of Csf1 op / Csf1 op mice. 41 In previous studies, we identified a 3.13-kb promoter and first intron fragment of mouse CSF-1 gene that conferred an essentially normal tissue-specific and developmental CSF-1 expression pattern.…”

Section: Discussionmentioning

confidence: 99%

“…18,27 csCSF-1 is expressed in all cell types examined that express soluble CSF-1, including fibroblasts and osteoblasts. 18,[24][25][26][27][28][29]36,37 It has been shown to support macrophage proliferation 25,38 and the formation of multinucleated osteoclastlike cells in vitro 37,39,40 and in vivo. 41 csCSF-1 was proposed to play adhesion molecule-like roles in its interaction with the CSF-1 receptor (CSF-1R) on leukemic cells in a culture system.…”

Section: Introductionmentioning

confidence: 99%

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Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1–deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1

Zong

Sylvestre

et al. 2004

Blood

121

140

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The primary macrophage growth factor, colony-stimulating factor 1 (CSF-1), is expressed as a secreted glycoprotein or proteoglycan found in the circulation or as a biologically active cell surface glycoprotein (csCSF-1). To investigate the in vivo roles of csCSF-1, we created mice that exclusively express csCSF-1, in a normal tissue-specific and developmental manner, by transgenic expression of csCSF-1 in the CSF-1-deficient osteopetrotic (Csf1 op / Csf1 op ) background. The gross defects of Csf1 op /Csf1 op mice, including growth retardation, failure of tooth eruption, and abnormal male and female reproductive functions were corrected. Macrophage densities in perinatal liver, bladder, sublinguinal salivary gland, kidney cortex, dermis, and synovial membrane were completely restored, whereas only partial or no restoration was achieved in adult liver, adrenal gland, kidney medulla, spleen, peritoneal cavity, and intestine. Residual osteopetrosis, significantly delayed trabecular bone resorption in the subepiphyseal region of the long bone, and incomplete correction of the hematologic abnormalities in the peripheral blood, bone marrow, and spleens of CSF-1-deficient mice were also found in mice exclusively expressing csCSF-1. These data suggest that although csCSF-1 alone is able to normalize several aspects of development in IntroductionColony-stimulating factor 1 (CSF-1), also known as macrophage CSF, is the primary regulator of the mononuclear phagocyte lineage and regulates cells of the female reproductive tract. [1][2][3][4][5][6] All effects of CSF-1 are mediated by a high-affinity receptor tyrosine kinase 7-10 encoded by the c-fms proto-oncogene. 11 At least 5 mature human or mouse CSF-1 mRNAs (4.0 kb, 3.0 kb, 2.3 kb, 1.9 kb, and 1.6 kb) resulting from alternative splicing in exon 6 and the alternative usages of the 3Ј-untranslated region exons 9 and 10, [12][13][14][15][16][17][18] have been shown to encode 3 isoforms of the CSF-1 protein: a secreted glycoprotein, 19-21 a secreted proteoglycan, 22,23 and a biologically active membrane-spanning cell surface glycoprotein 18,[24][25][26][27][28][29] (for a review, see Stanley 30 ).The primary source of the circulating proteoglycan and glycoprotein CSF-1 is thought to be the endothelial cells that line the small blood vessels (for a review, see Roth and Stanley 31 ). CSF-1 is also synthesized locally, 32 for example, by osteoblasts 33,34 and by uterine epithelial cells. 3 It has been suggested that regulation at particular tissue sites is mediated by local synthesis of the membrane-spanning, cell surface CSF-1 (csCSF-1), and/or selective sequestration of the secreted proteoglycan CSF-1 (spCSF-1). 22,23,35 The csCSF-1 is encoded by a truncated mRNA in which part of the exon 6 sequence encoding the fragment containing the unique glycosaminoglycan addition site and the proteolytic cleavage sites used to release the secreted isoforms has been spliced out ( Figure 1A). 18,27 csCSF-1 is expressed in all cell types examined that express soluble CSF-1, including fib...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1–deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1

Zong

Sylvestre

et al. 2004

Blood

121

140

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“…(32) Moreover, Itoh et al have shown that PTH up-regulates mRNA expression of RANKL but down-regulates mRNA expression of its decoy receptor OPG in human osteosarcoma SaOS-4/3 cells highly expressing recombinant PTH/PTH-related peptide (PTHrP) receptors. (33) In this study, we killed animals at 22-28 h after the last injection of PTH or vehicle. To determine whether we may have missed any early effects of PTH on gene expression of these markers, we examined the effects of shorter treatments with PTH for 1, 3, 6, and 24 h and found that PTH did not significantly change gene expression before 24 h (data not shown).…”

Section: Skeletal-site Specific Anabolic Action Of Pthmentioning

confidence: 99%

Anabolic Action of Parathyroid Hormone Is Skeletal Site Specific at the Tissue and Cellular Levels in Mice

Iida-Klein

Zhou

et al. 2002

Journal of Bone and Mineral Research

135

118

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The cellular and molecular events triggering the anabolic response of the skeleton to exogenous parathyroid hormone (PTH) are not well understood. Despite the numerous bone mass studies in rats, few data are available for mice. Therefore, we treated 10-week-old female intact C57BL/6J mice with human PTH(1-34) delivered subcutaneously at a dose of 40 g/kg per day 5 days a week for 3 weeks and 7 weeks. Bone mineral density (BMD) of total bone, femur, tibia, and lumbar vertebrae was measured weekly by PIXImus. Bone turnover was examined by histomorphometry, and gene expression of bone formation and resorption markers and osteoclastogenesis regulators in the excised femur and tibia was assessed by reverse-transcription polymerase chain reaction (RT-PCR) at 3 weeks and 7 weeks. The PTH-stimulated increase in BMD was more prominent in the tibia and femur than in the lumbar vertebrae, with an anabolic effect detected within 1-2 weeks and BMD continuing to increase. The appearance of a detectable PTH-stimulated increase in BMD was slower in the lumbar vertebrae where the increase was only significant after 7 weeks of treatment. Histomorphometric analysis of the proximal tibia at both 3 weeks and 7 weeks indicated significant time-dependent increases in trabecular area, trabecular number, trabecular and cortical widths, and osteoblast and osteoid perimeters. In the lumbar vertebrae, these stimulatory effects of PTH on trabecular area, trabecular number, and cortical width were smaller and not detected until 7 weeks. PTH-stimulated increases in bone turnover were evident by increased gene expression of osteocalcin (

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“…Encoded by a single gene, M-CSF contains five mature alternative transcripts. Under pathological conditions, there are at least three isoforms of M-CSF [7]: soluble M-CSF (s-M-CSF), membrane-bound M-CSF (m-M-CSF) and proteglycan-bound M-CSF (PG-M-CSF), which have been generated from these transcripts through co-and post-translational modifications. Different kinds of M-CSF isoforms are found in different cell types and under various conditions of stimulation.…”

Section: Introductionmentioning

confidence: 99%

Nuclear M-CSF Accelerates DNA Replication and Cell Proliferation in HeLa Human Cervical Cancer Cells

Tu¹

2017

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Macrophage colony-stimulating factor (M-CSF), also named colony-stimulating factor-1 (CSF-1), plays an important role in the process of proliferation and differentiation of the monocyte/macrophage lineage cells. Commonly, it is not easy to measure the expression of cellular M-CSF. However, recent studies have shown that M-CSF can be expressed at a high level in the cytoplasm and nuclei of some kinds of malignant tumors, which related to the poor prognosis. To explore the role and mechanism of nuclear M-CSF, in the present study we constructed the pCMV/nuc/M-CSF vector and transfected it into human HeLa nuclei. The results from our previous study indicated, M-CSF was stably expressed in HeLa nuclei, which were used as a model to determine the nuclear effects of M-CSF. There was a higher percentage of replicating nuclei in the transfected pCMV/nuc/M-CSF HeLa cells both in phase G1 and S. According to the data from the cell doubling time, antisense oligonucleotides and the experiments of the transplanted tumor in nude mice, nuclear M-CSF could promote the cell proliferation of HeLa cells both in vivo and in vitro. In conclusion, nuclear M-CSF could accelerate DNA replication and cell proliferation of cervical carcinoma.

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Importance of Membrane- or Matrix-Associated Forms of M-CSF and RANKL/ODF in Osteoclastogenesis Supported by SaOS-4/3 Cells Expressing Recombinant PTH/PTHrP Receptors

Abstract: SaOS

Cited by 84 publications

References 39 publications

Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1–deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1

Incomplete restoration of colony-stimulating factor 1 (CSF-1) function in CSF-1–deficient Csf1op/Csf1op mice by transgenic expression of cell surface CSF-1

Anabolic Action of Parathyroid Hormone Is Skeletal Site Specific at the Tissue and Cellular Levels in Mice

Nuclear M-CSF Accelerates DNA Replication and Cell Proliferation in HeLa Human Cervical Cancer Cells

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