The Experts below are selected from a list of 24438 Experts worldwide ranked by ideXlab platform
Osamu Suzuki - One of the best experts on this subject based on the ideXlab platform.
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elevated extraCellular calcium stimulates secretion of bone morphogenetic protein 2 by a Macrophage Cell Line
2006Co-Authors: Yoshitomo Honda, Takahisa Anada, Shinji Kamakura, Masanori Nakamura, Shunji Sugawara, Osamu SuzukiAbstract:Abstract It has been suggested that Macrophages and multinucleated giant Cells are responsible for phagocytosis of resorbable calcium phosphate (CaP) compounds implanted in bone defects. However, function of Macrophages around the CaP, if continuously exposed to various concentration of extraCellular calcium ions ([Ca 2+ ] o ), is still unknown. The present study showed that when resorbable octacalcium phosphate was implanted in mouse calvaria, Macrophage-like Cells were observed around the implant during bone formation. Then, experiments were designed to investigate whether secretion of bone morphogenetic protein 2 (BMP-2) is enhanced by extraCellular calcium ions in a Macrophage Cell Line (J774A.1) in vitro. The mRNA expression and the secretion of BMP-2 in J774A.1 Cells were significantly increased when incubated in the medium with [Ca 2+ ] o up to 14 mM. The promotion of mRNA expression was maintained even when incubated with a small amount of minute CaP crystals. The present results suggest that [Ca 2+ ] o above physiological concentration may stimulate Macrophages to induce osteogenic cytokine, such as BMP-2, for bone formation by osteoblasts.
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elevated extraCellular calcium stimulates secretion of bone morphogenetic protein 2 by a Macrophage Cell Line
2006Co-Authors: Yoshitomo Honda, Takahisa Anada, Shinji Kamakura, Masanori Nakamura, Shunji Sugawara, Osamu SuzukiAbstract:It has been suggested that Macrophages and multinucleated giant Cells are responsible for phagocytosis of resorbable calcium phosphate (CaP) compounds implanted in bone defects. However, function of Macrophages around the CaP, if continuously exposed to various concentration of extraCellular calcium ions ([Ca(2+)](o)), is still unknown. The present study showed that when resorbable octacalcium phosphate was implanted in mouse calvaria, Macrophage-like Cells were observed around the implant during bone formation. Then, experiments were designed to investigate whether secretion of bone morphogenetic protein 2 (BMP-2) is enhanced by [Ca(2+)](o) in a Macrophage Cell Line (J774A.1) in vitro. The mRNA expression and the secretion of BMP-2 in J774A.1 Cells were significantly increased when incubated in the medium with [Ca(2+)](o) up to 14mM. The promotion of mRNA expression was maintained even when incubated with a small amount of minute CaP crystals. The present results suggest that [Ca(2+)](o) above physiological concentration may stimulate Macrophages to induce osteogenic cytokine, such as BMP-2, for bone formation by osteoblast.
Yoshitomo Honda - One of the best experts on this subject based on the ideXlab platform.
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elevated extraCellular calcium stimulates secretion of bone morphogenetic protein 2 by a Macrophage Cell Line
2006Co-Authors: Yoshitomo Honda, Takahisa Anada, Shinji Kamakura, Masanori Nakamura, Shunji Sugawara, Osamu SuzukiAbstract:Abstract It has been suggested that Macrophages and multinucleated giant Cells are responsible for phagocytosis of resorbable calcium phosphate (CaP) compounds implanted in bone defects. However, function of Macrophages around the CaP, if continuously exposed to various concentration of extraCellular calcium ions ([Ca 2+ ] o ), is still unknown. The present study showed that when resorbable octacalcium phosphate was implanted in mouse calvaria, Macrophage-like Cells were observed around the implant during bone formation. Then, experiments were designed to investigate whether secretion of bone morphogenetic protein 2 (BMP-2) is enhanced by extraCellular calcium ions in a Macrophage Cell Line (J774A.1) in vitro. The mRNA expression and the secretion of BMP-2 in J774A.1 Cells were significantly increased when incubated in the medium with [Ca 2+ ] o up to 14 mM. The promotion of mRNA expression was maintained even when incubated with a small amount of minute CaP crystals. The present results suggest that [Ca 2+ ] o above physiological concentration may stimulate Macrophages to induce osteogenic cytokine, such as BMP-2, for bone formation by osteoblasts.
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elevated extraCellular calcium stimulates secretion of bone morphogenetic protein 2 by a Macrophage Cell Line
2006Co-Authors: Yoshitomo Honda, Takahisa Anada, Shinji Kamakura, Masanori Nakamura, Shunji Sugawara, Osamu SuzukiAbstract:It has been suggested that Macrophages and multinucleated giant Cells are responsible for phagocytosis of resorbable calcium phosphate (CaP) compounds implanted in bone defects. However, function of Macrophages around the CaP, if continuously exposed to various concentration of extraCellular calcium ions ([Ca(2+)](o)), is still unknown. The present study showed that when resorbable octacalcium phosphate was implanted in mouse calvaria, Macrophage-like Cells were observed around the implant during bone formation. Then, experiments were designed to investigate whether secretion of bone morphogenetic protein 2 (BMP-2) is enhanced by [Ca(2+)](o) in a Macrophage Cell Line (J774A.1) in vitro. The mRNA expression and the secretion of BMP-2 in J774A.1 Cells were significantly increased when incubated in the medium with [Ca(2+)](o) up to 14mM. The promotion of mRNA expression was maintained even when incubated with a small amount of minute CaP crystals. The present results suggest that [Ca(2+)](o) above physiological concentration may stimulate Macrophages to induce osteogenic cytokine, such as BMP-2, for bone formation by osteoblast.
Sidney M Morris - One of the best experts on this subject based on the ideXlab platform.
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novel actions of aspirin and sodium salicylate discordant effects on nitric oxide synthesis and induction of nitric oxide synthase mrna in a murine Macrophage Cell Line
1996Co-Authors: Diane Kepkalenhart, Lichun Chen, Sidney M MorrisAbstract:Aspirin and sodium salicylate each inhibit to a similar extent the production of nitric oxide (NO) in the RAW 264.7 murine Macrophage Cell Line following stimulation by either lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma). The similar potencies of aspirin and sodium salicylate indicate that acetylation of Cellular macromolecules is not essential for the observed effects. The failure of added prostaglandin E2 to overcome the effects of aspirin or sodium salicylate indicates that these effects are not simply the result of inhibition of prostaglandin synthesis. The inhibition of NO production occurs irrespective of the effect of these agents on induction of nitric oxide synthase (iNOS) mRNA by LPS or IFN-gamma. Aspirin and sodium salicylate inhibit iNOS mRNA induction in LPS-stimulated Cells but enhance iNOS mRNA induction in IFN-gamma-stimulated Cells. In contrast, these agents consistently inhibit induction of argininosuccinate synthetase mRNA in both LPS- and IFN-gamma-stimulated Cells. Concentrations of aspirin in the 3-10 mM range inhibit induced NO production and expression of iNOS protein without inhibiting induction of iNOS mRNA. Discordances between effects on NO synthesis and induction of iNOS mRNA indicate that aspirin and sodium salicylate have multiple sites of action in their effects on pathways that are involved in the production of NO by stimulated RAW 264.7 Cells.
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coinduction of nitric oxide synthase and argininosuccinate synthetase in a murine Macrophage Cell Line implications for regulation of nitric oxide production
1994Co-Authors: Andreas K Nussler, Timothy R Billiar, Zhize Liu, Sidney M MorrisAbstract:In Macrophages and other Cell types, bacterial lipopolysaccharide and certain cytokines stimulate nitric oxide (NO) production via expression of the inducible isoform of nitric oxide synthase (NOS). CitrulLine, which is the coproduct of NOS-catalyzed metabolism of arginine, can be recycled to arginine by the action of argininosuccinate synthetase and argininosuccinate lyase, which are present at high levels in hepatocytes and renal tubular Cells but normally at very low levels in other Cell types such as Macrophages. The present study demonstrates that lipopolysaccharide and interferon-gamma, which induce NOS in the murine Macrophage Cell Line RAW 264.7, also coinduce activity and mRNA for argininosuccinate synthetase, which is limiting for arginine synthesis. Argininosuccinate lyase activity and mRNA abundance are unaffected. Induction of argininosuccinate synthetase is not blocked by NG-monomethyl-L-arginine, a potent inhibitor of NOS, indicating that argininosuccinate synthetase induction is not the consequence of depleting Cellular arginine levels by NOS. Because plasma levels of arginine are limiting for NO synthesis, enhanced Cellular capacity to regenerate arginine from citrulLine could play a significant role in regulating NO production, especially under conditions where the inducible isoform of NOS is expressed.
Hyungjoo Kwon - One of the best experts on this subject based on the ideXlab platform.
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nf kappab dependent regulation of matrix metalloproteinase 9 gene expression by lipopolysaccharide in a Macrophage Cell Line raw 264 7
2007Co-Authors: Jae Won Rhee, Keunwook Lee, Young Hee Lee, Hyungjoo Kwon, Dongbum Kim, Okhee Jeon, Doosik KimAbstract:Matrix metalloproteinase-9 (MMP-9) plays a pivotal role in the turnover of extraCellular matrix (ECM) and in the migration of normal and tumor Cells in response to normal physiologic and numerous pathologic conditions. Here, we show that the transcription of the MMP-9 gene is induced by lipopolysaccharide (LPS) stimulation in Cells of a Macrophage Lineage (RAW 264.7 Cells). We provide evidence that the NF-kappaB binding site of the MMP-9 gene contributes to its expression in the LPS-signaling pathway, since mutation of NF-kappaB binding site of MMP-9 promoter leads to a dramatic reduction in MMP-9 promoter activation. In addition, the degradation of IkappaBalpha, and the presences of myeloid differentiation protein (MyD88) and tumor necrosis factor receptor-associated kinase 6 (TRAF6) were found to be required for LPS-activated MMP-9 expression. Chromatin immunoprecipitation (ChIP) assays showed that functional interaction between NF-kappaB and the MMP-9 promoter element is necessary for LPS-activated MMP-9 induction in RAW 264.7 Cells. In conclusion, our observations demonstrate that NF-kappaB contributes to LPS-induced MMP-9 gene expression in a mouse Macrophage Cell Line.
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pyrrolidine dithiocarbamate induced Macrophage inflammatory protein 2 gene expression is nf κb independent but c jun dependent in Macrophage Cell Line raw 264 7
2005Co-Authors: Wernjoo Sohn, Keunwook Lee, Young Hee Lee, Jung Ho Han, Yongkyoung Choe, Doosik Kim, Hyungjoo KwonAbstract:Pyrrolidine dithiocarbamate (PDTC) is a stable compound that acts as antioxidant or prooxidant, and is widely used to inhibit the activation of NF-κB. PDTC was also reported to activate NF-κB depending on its dose and metal ions in PC12 Cells. In this work, we demonstrated a working mechanism of PDTC and its effects on the proinflammatory cytokine gene expression in a mouse Macrophage Cell Line, RAW 264.7. PDTC alone induced NF-κB-independent MIP-2 promoter activation that can be assessed by transient transfection and confocal image analysis. The involvement of AP-1 transcription factor was noticed by promoter deletion/site-specific mutation analysis and electrophoretic mobility shift assay (EMSA). Among three different mitogen-activated protein kinase (MAPK) pathways tested, only the stress-activated protein kinase (SAPK)/Jun N-terminal kinase (JNK) pathway was significantly activated in RAW 264.7 Cells after the stimulation with PDTC. Using pathway-specific inhibitors, we found that the SAPK/JNK pathway is clearly associated with PDTC-induced MIP-2 gene expression. Our experimental results indicate that PDTC-induced proinflammatory cytokine expressions are mediated by SAPK/JNK pathway, which activates AP-1.
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nf κb and c jun dependent regulation of human cytomegalovirus immediate early gene enhancer promoter in response to lipopolysaccharide and bacterial cpg oligodeoxynucleotides in Macrophage Cell Line raw 264 7
2004Co-Authors: Young Hee Lee, Wernjoo Sohn, Doosik Kim, Hyungjoo KwonAbstract:The cytomegalovirus immediate-early (CMV IE) gene enhancer/promoter regulates the expression of immediate-early gene products and initiation of CMV replication. TNF-α and lipopolysaccharide (LPS) strongly activate the promoter, possibly involving NF-κB. CpG-oligodeoxynucleotides (CpG-ODNs), which contain unmethylated CpG dinucleotides in the context of particular base sequences, have gained attention because of their stimulating effects, via NF-κB, which have a strong innate immune response. To study the effects of LPS and CpG-ODNs, as well as the mechanisms of their actions regarding CMV IE enhancer/promoter activation, we used a Macrophage Cell Line, RAW 264.7. Stimulation of the Cells with LPS or CpG-ODNs resulted in the activation of the CMV IE enhancer/promoter. We examined the involvement of NF-κB and c-Jun transcription factors by promoter deletion/site-specific mutation analysis and ectopic expression, and found them to have additive effects. Involvement of myeloid differentiation protein, an upstream regulator of NF-κB and c-Jun, was also investigated. Experimental results indicate that both LPS-induced and CpG-ODN-induced activations of CMV IE enhancer/promoter are mediated by Toll-like receptor signaling molecules. Several Lines of evidence suggest the potential contribution of bacterial infection in CMV reactivation along with the potential application of CpG-ODNs in gene therapy as a stimulator for the optimal expression of target genes under the control of the CMV IE enhancer/promoter.
Louis J Ignarro - One of the best experts on this subject based on the ideXlab platform.
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inducible nitric oxide synthase from a rat alveolar Macrophage Cell Line is inhibited by nitric oxide
1993Co-Authors: J M Griscavage, Norma E Rogers, Michael P Sherman, Louis J IgnarroAbstract:The objective of this study was to determine whether inducible nitric oxide (NO) synthase from a rat alveolar Macrophage Cell Line (NR8383) activated by LPS plus IFN-gamma could be regulated by NO, one of the two products of the enzymatic reaction. This study was based on previous observations in this laboratory that NO is a negative feedback modulator of constitutive NO synthase from rat cerebellum. NO synthase activity was determined by monitoring the formation of 3H-L-citrulLine from 3H-L-arginine in the presence of added cofactors. NO synthase catalyzed the conversion of L-arginine to equimolar quantities of NO and L-citrulLine. NO and S-nitrosothiols inhibited NO synthase activity and this effect was enhanced by superoxide dismutase and attenuated by oxyhemoglobin. Nitrite and nitrate, the oxidation products of NO, as well as L-citrulLine, the amino acid end-product, produced no significant effects on NO synthase activity. The inhibitory effect of NO on NO synthase appeared to be partially reversible upon addition of oxyhemoglobin. The inhibitory effect of NO was mimicked by other heme ligands including carbon monoxide, cyanide, and manganese-protoporphyrin IX. These observations indicate that (1) enzyme-bound heme plays a mechanistic role in the catalytic conversion of L-arginine to NO plus L-citrulLine; (2) NO may function as a negative feedback modulator of inducible NO synthase by interacting with enzyme-bound heme; and (3) negative feedback modulation by NO may represent a mechanism by which the potentially toxic L-arginine-NO pathway in activated alveolar Macrophages is turned off.
