Direct stimulation of osteoclastogenesis by MIP-1alpha: evidence obtained from studies using RAW264 cell clone highly responsive to RANKL

Macrophage inflammatory protein-1alpha (MIP-1alpha) is a member of the CC chemokines. We have previously reported the use of a whole bone marrow culture system to show that MIP-1alpha stimulates the formation of osteoclast-like multinucleated cells. Here we use rat bone marrow cells deprived of stromal cells, and clones obtained from murine macrophage-like cell line RAW264 to show that MIP-1alpha acts directly on cells in osteoclast lineage. We obtained several types of RAW264 cell clones, one of these clones, designated as RAW264 cell D clone (D clone), showed an extremely high response to receptor activator of NFkappaB ligand (RANKL) and tumor necrosis factor-alpha (TNF-alpha), while the other clone, RAW264 cell N clone (N clone), demonstrated no response to RANKL or TNF-alpha. Although both clones expressed receptor activator NFkappaB (RANK) before being stimulated for differentiation, only the D clone expressed cathepsin K when cells were stimulated to differentiate to osteoclasts. MIP-1alpha stimulated the formation of mononuclear preosteoclast-like cells from rat bone marrow cells deprived of stromal cells. MIP-1alpha also stimulated formation of osteoclast-like multinucleated cells from the D clone, when these cells were stimulated with RANKL and TNF-alpha. These findings provide strong evidence to show that MIP-1alpha acts directly on cells in the osteoclast lineage to stimulate osteoclastogenesis. Furthermore, pretreatment of RAW264 cell D clone with MIP-1alpha significantly induced adhesion properties of these cells to primary osteoblasts, suggesting a crucial role for MIP-1alpha in the regulation of the interaction between osteoclast precursors and osteoblasts in osteoclastogenesis.

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Effects of berberine on differentiation and bone resorption of osteoclasts derived from rat bone marrow cells

Journal of Chinese Integrative Medicine ◽

10.3736/jcim20090408 ◽

2009 ◽

Vol 7 (4) ◽

pp. 342-348 ◽

Cited By ~ 13

Author(s):

P Wei

Keyword(s):

Bone Marrow ◽

Bone Resorption ◽

Bone Marrow Cells ◽

Rat Bone ◽

Marrow Cells

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Glucosamine Protects Rat Bone Marrow Cells Against Cisplatin-induced Genotoxicity and Cytotoxicity

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520619666190704164126 ◽

2019 ◽

Vol 19 (14) ◽

pp. 1695-1702 ◽

Cited By ~ 1

Author(s):

Mohsen Cheki ◽

Salman Jafari ◽

Masoud Najafi ◽

Aziz Mahmoudzadeh

Keyword(s):

Bone Marrow ◽

Bone Marrow Cells ◽

Micronucleus Assay ◽

Ros Generation ◽

Polychromatic Erythrocytes ◽

Hematological Analysis ◽

Antagonistic Potential ◽

Harmful Effects ◽

Rat Bone ◽

Marrow Cells

Background and Objective: Glucosamine is a widely prescribed dietary supplement used in the treatment of osteoarthritis. In the present study, the chemoprotectant ability of glucosamine was evaluated against cisplatin-induced genotoxicity and cytotoxicity in rat bone marrow cells. Methods: Glucosamine was orally administrated to rats at doses of 75 and 150 mg/kg body weight for seven consecutive days. On the seventh day, the rats were treated with a single injection of cisplatin (5 mg/kg, i.p.) at 1h after the last oral administration. The cisplatin antagonistic potential of glucosamine was assessed by micronucleus assay, Reactive Oxygen Species (ROS) level analysis, hematological analysis, and flow cytometry. Results: Glucosamine administration to cisplatin-treated rats significantly decreased the frequencies of Micronucleated Polychromatic Erythrocytes (MnPCEs) and Micronucleated Normchromatic Erythrocytes (MnNCEs), and also increased PCE/(PCE+NCE) ratio in bone marrow cells. Furthermore, treatment of rats with glucosamine before cisplatin significantly inhibited apoptosis, necrosis and ROS generation in bone marrow cells, and also increased red blood cells count in peripheral blood. Conclusion: This study shows glucosamine to be a new effective chemoprotector against cisplatin-induced DNA damage and apoptosis in rat bone marrow cells. The results of this study may be helpful in reducing the harmful effects of cisplatin-based chemotherapy in the future.

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The Ratio of sTfR/Ferritin is Associated with the Expression Level of TfR in Rat Bone Marrow Cells After Endurance Exercise

Biological Trace Element Research ◽

10.1007/s12011-011-9312-6 ◽

2011 ◽

Vol 147 (1-3) ◽

pp. 261-266 ◽

Cited By ~ 4

Author(s):

Ye Tian ◽

Jiexiu Zhao ◽

Binxiu Zhao ◽

Qi Gao ◽

Jincheng Xu ◽

...

Keyword(s):

Bone Marrow ◽

Endurance Exercise ◽

Bone Marrow Cells ◽

Expression Level ◽

Rat Bone ◽

Marrow Cells

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Osteoblastic differentiation of cultured rat bone marrow cells on hydroxyapatite with different surface topography

Dental Materials ◽

10.1016/s0109-5641(03)00024-1 ◽

2003 ◽

Vol 19 (8) ◽

pp. 768-772 ◽

Cited By ~ 83

Author(s):

Adalberto L Rosa ◽

Márcio M Beloti ◽

Richard van Noort

Keyword(s):

Bone Marrow ◽

Surface Topography ◽

Bone Marrow Cells ◽

Osteoblastic Differentiation ◽

Rat Bone ◽

Marrow Cells

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Bisecting GlcNAc structure is implicated in suppression of stroma-dependent haemopoiesis in transgenic mice expressing N-acetylglucosaminyltransferase III

Biochemical Journal ◽

10.1042/bj3310733 ◽

1998 ◽

Vol 331 (3) ◽

pp. 733-742 ◽

Cited By ~ 8

Author(s):

Masafumi YOSHIMURA ◽

Yoshito IHARA ◽

Tetsuo NISHIURA ◽

Yu OKAJIMA ◽

Megumu OGAWA ◽

...

Keyword(s):

Bone Marrow ◽

Transgenic Mice ◽

Stromal Cells ◽

Bone Marrow Cells ◽

Adherent Cell ◽

Wild Type ◽

Spleen Cells ◽

Bisecting Glcnac ◽

Marrow Cells

Several sugar structures have been reported to be necessary for haemopoiesis. We analysed the haematological phenotypes of transgenic mice expressing β-1,4 N-acetylglucosaminyltransferase III (GnT-III), which forms bisecting N-acetylglucosamine on asparagine-linked oligosaccharides. In the transgenic mice, the GnT-III activity was elevated in bone marrow, spleen and peripheral blood and in isolated mononuclear cells from these tissues, whereas no activity was found in these tissues of wild-type mice. Stromal cells after long-term cultures of transgenic-derived bone marrow and spleen cells also showed elevated GnT-III activity, compared with an undetectable activity in wild-type stromal cells. As judged by HPLC analysis, lectin blotting and lectin cytotoxicity assay, bisecting GlcNAc residues were increased on both blood cells and stromal cells from bone marrow and spleen in transgenic mice. The transgenic mice displayed spleen atrophy, hypocellular bone marrow and pancytopenia. Bone marrow cells and spleen cells from transgenic mice produced fewer haemopoietic colonies. After lethal irradiation followed by bone marrow transplantation, transgenic recipient mice showed pancytopenia compared with wild-type recipient mice. Bone marrow cells from transgenic donors gave haematological reconstitution at the same level as wild-type donor cells. In addition, non-adherent cell production was decreased in long-term bone marrow cell cultures of transgenic mice. Collectively these results indicate that the stroma-supported haemopoiesis is compromised in transgenic mice expressing GnT-III, providing the first demonstration that the N-glycans have some significant roles in stroma-dependent haemopoiesis.

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