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Mouse Bone Marrow Cells (mouse + bone_marrow_cell)
Selected AbstractsThe Balance Between Concurrent Activation of ERs and PPARs Determines Daidzein-Induced Osteogenesis and Adipogenesis,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 5 2004ZhiChao Dang PhD Abstract The soy phytoestrogen daidzein has biphasic dose responses, but the underlying mechanisms are not yet clear. Transcriptional and biochemical data show that PPARs, in addition to ERs, are molecular targets of daidzein, which divergently regulates osteogenesis and adipogenesis. Dose responses are the result of a balance among PPARs and between ERs and PPARs. Introduction: Soy phytoestrogens have been used for the purposes of treatment and prevention of osteoporosis. Biphasic dose responses of daidzein, one of the main soy phytoestrogens, have long been recognized, but the underlying molecular mechanisms of action are not yet clear. Materials and Methods: Mouse bone marrow cells and mouse osteoprogenitor KS483 cells that concurrently differentiate into osteoblasts and adipocytes were cultured. Biochemical measurement of alkaline phosphatase (ALP) activity, RT-PCR, and gene reporter assays were used in this study. Results: Daidzein, one of the major soy phytoestrogens, had biphasic effects on osteogenesis and adipogenesis. Daidzein stimulated osteogenesis (ALP activity and nodule formation) and decreased adipogenesis (the number of adipocytes) at concentrations below 20 ,M, whereas it inhibited osteogenesis and stimulated adipogenesis at concentrations higher than 30 ,M. When estrogen receptors (ERs) were blocked by ICI182,780, daidzein-induced effects were not biphasic. A decrease in osteogenesis and an increase in adipogenesis were observed at the concentrations higher than 20 and 10 ,M, respectively. In addition to ERs, daidzein transactivated not only peroxisome proliferator-activate receptor , (PPAR,), but also PPAR, and PPAR, at micromolar concentrations. Activation of PPAR, had no direct effects on osteogenesis and adipogenesis. In contrast, activation of PPAR, stimulated osteogenesis but had no effects on adipogenesis, whereas PPAR, inhibited osteogenesis and stimulated adipogenesis. Transfection experiments show that an activation of PPAR, or PPAR, by daidzein downregulated its estrogenic transcriptional activity, whereas activation of PPAR, upregulated its estrogenic transcriptional activity. Activation of ER, or ER, by daidzein downregulated PPAR, transcriptional activity but had no influence on PPAR, or PPAR, transcriptional activity. Conclusions: Daidzein at micromolar concentrations concurrently activates different amounts of ERs and PPARs, and the balance of the divergent actions of ERs and PPARs determines daidzein-induced osteogenesis and adipogenesis. [source] Cytogenetic effects of commercial formulations of deltamethrin and/or isoproturon on human peripheral lymphocytes and mouse bone marrow cellsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 8 2007Lalit K.S. Chauhan Abstract The cytogenetic effects of deltamethrin (DEL) and/or isoproturon (ISO) were examined in human lymphocytes and mouse bone marrow cells. Peripheral lymphocytes were exposed to DEL (2.5, 5, 10, or 20 ,M), ISO (25, 50, 100, or 200,M), or DEL + ISO (2.5 + 25, 5 + 50, 10 + 100, or 20 + 200 ,M) and cytogenic effects were evaluated via chromosomal aberrations (CA) and the cytokinesis-block micronucleus assay (CBMN). Mice were orally gavaged to single dose of DEL (6.6 mg/kg), ISO (670 mg/kg), or DEL+ISO (6.6 + 670 mg/kg) for 24 hr or to DEL (3.3 mg/kg/day), ISO (330 mg/kg/day), or DEL + ISO (3.3 + 330 mg/kg/day) for 30 days and analyzed for CA. DEL induced a significant frequency of CA at 10 ,M whereas ISO (25,100,M) alone, or in combination with DEL, did not show any significant effect. Micronucleus (MN) induction was observed to be concentration-dependent though significant frequencies were observed at 5 ,M DEL, 100 ,M ISO, or 5 + 50 ,M DEL + ISO. In mice, DEL inhibited the mitotic index (MI) significantly (P < 0.001) at 24 hr while ISO alone, or in combination with DEL, did not cause any statistically significant effect. Following a 24 hr exposure, DEL and ISO alone induced significant (P < 0.01) frequencies of CA, whereas DEL + ISO in combination did not. Furthermore, 30 days exposure of ISO significantly inhibited the MI (P < 0.02 or < 0.01) and induced CA while DEL alone, or in combination with ISO, resulted in no significant effect on CA or the MI. The present findings indicate that the in vitro and in vivo exposure of a commercial formulation of DEL can cause genotoxic effects in mammals. However, the coexposure of DEL and ISO did not show additive effects, but instead demonstrated somewhat reduced genotoxicity. Environ. Mol. Mutagen., 2007. © 2007 Wiley-Liss, Inc. [source] Cancer stem cells in leukemia, recent advancesJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2007Gang-Ming Zou The history of stem cell research was started in the early 1900s in Europe where the researcher realized that various types of blood cells came from a particular "stem cells." However, it was not until 1963 that the first quantitative description of the self-renewal activities of transplanted mouse bone marrow cells were documented by Canadian scientist Ernest A McCulloch and James E Till in Toronto. The concept of cancer stem cells has been used over 50 years ago; whereas the strong evidence for the existence of a Cancer Stem Cells was obtained recently. Consequently, there is increasing attention in recent year about cancer stem cells. The findings from recent studies support the concept that stem cells are integral to the development of several forms of human cancer. Changes in stem cell behavior can contribute to tumor formation. Leukemia is a cancer of blood-forming tissue, including the bone marrow and lymphatic system. Leukemic stem cells represent the cancer stem cells in the leukemia. In this review, we summarize the recent advance in the study of leukemic stem cells. J. Cell. Physiol. 213: 440,444, 2007. © 2007 Wiley-Liss, Inc. [source] Inhibitory effects of green tea polyphenol (,)-epigallocatechin gallate on the expression of matrix metalloproteinase-9 and on the formation of osteoclastsJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2004Jeong-Ho Yun Background:, Alveolar bone resorption is a characteristic feature of periodontal diseases and involves the removal of both the mineral and organic constituents of the bone matrix, which is caused by either multinucleated osteoclast cells or matrix metalloproteinases (MMPs). The gram-negative bacterium, Porphyromonas gingivalis has been reported to stimulate the activity and expression of several groups of MMPs, whereas (,)-epigallocatechin gallate (EGCG), the main constituent of green tea polyphenols, has been reported to have inhibitory effects on the activity and expression of MMPs. Objectives:, In the present study, we investigated the effects of the green tea polyphenol, EGCG, on the gene expression of osteoblast-derived MMP-2, -9 and -13, stimulated by P. gingivalis, and on the formation of osteoclasts. Methods:, The effect of EGCG on the gene expression of MMPs was examined by treating mouse calvarial primary osteoblastic cells with EGCG (20 µm) in the presence of sonicated P. gingivalis extracts. The transcription levels of MMP-2, -9 and -13 were assessed by reverse transcription-polymerase chain reaction (RT-PCR). The effect of EGCG on osteoclast formation was confirmed by tartrate-resistant acid phosphatase (TRAP) staining in a co-culture system of mouse bone marrow cells and calvarial primary osteoblastic cells. Results:, Treatment with the sonicated P. gingivalis extracts stimulated the expression of MMP-9 mRNA and this effect was significantly reduced by EGCG, whereas the transcription levels of MMP-2 and MMP-13 were not affected by either the sonicated P. gingivalis extracts or EGCG. In addition, EGCG significantly inhibited osteoclast formation in the co-culture system at a concentration of 20 µm. Conclusions:, These findings suggest that EGCG may prevent the alveolar bone resorption that occurs in periodontal diseases by inhibiting the expression of MMP-9 in osteoblasts and the formation of osteoclasts. [source] Expression of receptor activator of NF-kappa B ligand and osteoprotegerin in culture of human periodontal ligament cellsJOURNAL OF PERIODONTAL RESEARCH, Issue 6 2002Tomokazu Hasegawa The receptor activator of NF-kappa B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), are the important proteins implicated in osteoclastogenesis. In this study, we investigated the expressions of RANKL and OPG in cultured human periodontal ligament (PDL) cells and their roles in osteoclastogenesis. Northern blotting revealed that the OPG mRNA was down-regulated remarkably by application of 10,8 m one-alpha, 25-dihydroxyvitamin D3[1,25-(OH)2D3] and 10,7 m dexamethasone (Dex). In contrast, RANKL mRNA was up-regulated by the same treatment. Western blotting demonstrated decrease of OPG by the application of 1,25-(OH)2D3 and Dex. Tartrate-resistant acid phosphatase-positive multinuclear cells were markedly induced when the PDL cells were cocultured with mouse bone marrow cells in the presence of an anti-OPG antibody together with 1,25-(OH)2D3 and Dex. These results indicate that PDL cells synthesize both RANKL and OPG and that inactivation of OPG may play a key role in the differentiation of osteoclasts. [source] The role of LFA-1 in osteoclast development induced by co-cultures of mouse bone marrow cells and MC3T3-G2/PA6 cellsJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2002N. Tani-Ishii Interactions between leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM,1) influence the development of osteoclasts. However, little is known about how these adhesion molecules are involved in the process of osteoclast development. This study evaluated the role of LFA-1 and its ligands in osteoclast development and bone resorption. Co-cultures of bone marrow cells from LFA-1-deficient mice and MC3T3-G2/PA6 (PA6) cells were cultured in the presence of 1,,25(OH)2D3 and dexamethasone for 7 days. The number of TRAP-positive cells that were generated by bone marrow cells from LFA-1-deficient mice was smaller than that generated by bone marrow cells from wild-type mice. In addition, the bone-resorbing activity of osteoclast-like cells that were generated from LFA-1-deficient mice was lower than that generated by osteoclast-like cells from wild-type mice. Immunofluorescence flow cytometry showed that osteoclast stromal PA6 cells expressed the cell adhesion molecules, ICAM-1 and VCAM-1. When monoclonal antibodies to mice VCAM-1, CD11b or CD18 were added separately to the co-culture system, the number of TRAP-positive cells that were generated from LFA-1-deficient mice was 20,30% smaller than that generated from wild-type mice. The formation of TRAP-positive cells from both LFA-1 deficient and wild-type mice was especially inhibited by anti-CD18 antibody, in comparison to the addition of normal IgG serum. These results suggest that LFA-1 adhesion molecules play a role in osteoclast development by affecting adhesion between stromal cells and osteoclast progenitors before the occurrence of ODF-ODF receptor signaling. CD18 appears to be a key adhesion molecule in cell-to-cell contacts during the early stage of osteoclast development. [source] Pluchea lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity in Swiss albino miceJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2005Tamanna Jahangir Cadmium intoxication induces lipid peroxidation and causes oxidative damage to various tissues by altering antioxidant defence system enzymes. At 24h after treatment with a single intraperitoneal dose of cadmium chloride (5 mg kg,1), Swiss albino mice showed a significant increase in the levels of malanodialdehyde and xanthine oxidase (P<0.001), and a concomitant depletion of renal glutathione, catalase (P<0.001) and other antioxidant enzymes. CdCl2 also led to a simultaneous increase in micronuclei formation (P<0.001) and chromosomal aberrations (P<0.05) in mouse bone marrow cells. Oral pre-treatment with Pluchea lanceolata extract at doses of 100 and 200 mg kg,1 for 7 consecutive days before CdCl2 intoxication caused a significant reduction in malanodialdehyde formation and xanthine oxidase activity (P<0.001). A significant restoration of the activity of antioxidant defence system enzymes such as catalase, glutathione peroxidase (P<0.05), glutathione- S -transferase and glutathione reductase (P<0.001) was observed. A significant dose-dependent decrease in chromosomal aberrations and micronuclei formation was also observed (P<0.05). The results indicate that pre-treatment with P. lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity by altering antioxidant enzymes and reducing chromatid breaks and micronuclei formation. [source] Water extract of Cordyceps sinensis (WECS) inhibits the RANKL-induced osteoclast differentiationBIOFACTORS, Issue 2 2007Yoko Mizuha Abstract It has been reported that Cordyceps sinensis, a traditional Chinese medicine, has various pharmacological effects. The aim of this study was to clarify the effect of water extract of Cordyceps sinensis (WECS) on osteoclast differentiation in vitro. In mouse bone marrow cells and monocyte/macrophage cell line RAW264.7, WECS dose-dependently inhibited the receptor activator of nuclear factor kappa B (NF-,B) ligand (RANKL)-induced osteoclast differentiation by tartrate-resistant acid phosphatase (TRAP) staining. In fact, cytotoxic effect was not observed in the RAW264.7 cells treated with WECS. Moreover, the mRNA expression of osteoclast related genes (calcitonin receptor, cathepsin K, matrix metalloprotease 9 and nuclear factor of activated T cells c1) was also inhibited by WECS. Investigation of inhibitory mechanism by using electrophoretic mobility shift assay (EMSA) and Western blot analysis revealed that WECS inhibited the activation of NF-,B through the prevention of I,B, phosphorylation. In conclusion, the present results demonstrate for the first time that WECS is a potent inhibitor of the RANKL-induced osteoclast differentiation through a mechanism involving the NF-,B pathway. [source] | |||||||||||||