• The korean journal of orthodontics
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• v.21 no.1 s.33
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• pp.97-111
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• 1991

It is the aim of this study to investigate the effects of sodium fluoride and sodium orthovanadate upon the proliferation and activity of the osteoblast (MC3T3-E1 cells). MC3T3-E1 cells were cultured in $\alpha-MEM$ containing $10\%$ FBS and various concentration of sodium fluoride and sodium orthovanadate was appended to serum free media. DNA synthesis was examined through the $[^3H]$ thymidine incorporation into DNA. Collagen synthesis was examined through the $[^3H]$ proline incorporation into collagenase digestible protein and noncollagen protein. The following results were drawn; 1. Sodium fluoride stimulated the DNA synthesis of osteoblast significantly in dose-dependent manner within the concentration from $2{\mu}M$ to $10{\mu}M$ (P < 0.005). 2. Sodium orthovanadate stimulated the DNA synthesis of osteoblast significantly in dose-dependent manner within the concentration from $2{\mu}M\;to\;8{\mu}M$, however showed diminution at $10{\mu}M$ (P < 0.001). 3. Sodium fluoride and sodium orthovanadate stimulated the percent collagen synthesis of osteoblast significantly in dose-dependent manner within the concentration from $5{\mu}M$ to $10{\mu}M$ (P < 0.001). 4. Sodium fluoride and sodium orthovanadate stimulated the noncollagen synthesis of osteoblast significantly in dose-dependent manner within the concentration from $5{\mu}M\;to\;10{\mu}M$ (P < 0.001). In conclusion, sodium fluoride and sodium orthovanadate stimulate the proliferation and activity of osteoblast by stimulation of DNA synthesis and collagen and noncollagen synthesis in osteoblast.

• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.101-106
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• 1983

Vanadium is widely distributed in animal tissues and it is supposed to be a regulator of Na-K-ATPase activity. The effect of sodium orthovanadate on Na-K-ATPase activity in rabbit kidney was measured in vitro and compared with that of ouabain. The influence of sodium orthovanadate on the renal function of rabbits was also investigated. 1) Na-K-ATPase activity was decreased by sodium orthovandate at the concentrations of $10^{-7},\;10^{-6},\;10^{-5}\;and\;10^{-4}\;M$ to 73.89, 36.49, 6.50 and 4.99% of the control activity respectively. 2) Na-K-ATPase activity was decreased by ouabain at the concentrations of $10^{-4},\;10^{-3}\;and\;10^{-2}\;M$ to 69.52, 22.84 and 3.88% of the control activity respectively. 3) Urine volume, urinary excretion of $Na^+,\;K^+\;and\;Cl^-$, clearances of inulin and p-amino-hoppuric acid were decreased until after 60 minutes following the administration of sodium orthovanadate 0.5 mg/kg intravenously $Na^+\;reasorption$ rate was not changed and mean arterial pressure was significantly elevated during 60 minutes after the administration of sodium orthovanadate.

• The korean journal of orthodontics
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• v.24 no.1 s.44
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• pp.17-35
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• 1994

Vanadium is an essential trace element but has not been identified with a specific biogical role. To study the direct effects of vanadium on osteoblast, we incubated murin osteoblast-like (MC3T3-El) cells with various corcentration of vanadium oxide & sodium orthovanadate. This study was designed to investigate the effect of vanadium on DNA synthesis, alkaline phosphatase (ALP) activity, cAMP formation responsive to parathormone(PTH) and type I $\alpha$ 2 collagen ribonucleic acid (mRNA) level in murin osteoblast-like (MC3T3-El) cells. The cells were cultured in $\alpha-minimal$ essential medium$(\alpha-MEM)$ supplemented with $10\%$ fetal bovine serum (FBS) and then changed to $0.1\%$ FBS with various concenoation of vanadium oxide & sodium orthovanadate. Quiescent cultured MC3T3-El cells incubated for 24 hours with 2,5,10,15,20 ${\mu}M$ vanadium oxide incorporated $[^3H]Thymidine;$ every concentration showed increases in $[^3H]Thymidine$ incorporations dose dependant manner, the greatest response occurred at $20{\mu}M$. Quiescent cultured MC3T3-E1 cells incubated for 3days with 2,5,10,15,20 ${\mu}M$ vanadium oxide, for 2days with sodium orthovanadate and alkaline phosphatase was assayed with disodium phenyl phosphate as substrate. Vanadium oxide increased the alkaline phosphatase content in MC3T3-El cells at $2{\mu}M\;&\;6{\mu}M$ ; the greatest response occurred at $2{\mu}M$. But decreased at other content sodium orthovanadate increased alkaline phosphatase content in MC3T3-El cells at all concenoation ; the greatest response occurred at $4{\mu}M$. Quiescent cultured MC3T3-El cells incubated for 3days with $5,10{\mu}M$ vanadium oxide , with $5,8{\mu}M$ sodium orthovanadate and cAMP formation was measured by Radioimmunoassay(RIA). Vanadium oxide & sodium orthovanadate showed the tendency of inhibitory effects on cAMP responsiveness to PTH in MC3T3-El cells. Quiescent cultured MC3T3-El cells incubated for 24hours with $10,20{\mu}M$ vanadium oxide, with $5,10{\mu}M$ sodium orthovanadate and Type I $\alpha$ 2 collagen ribonucleic acid (mRNA) expression was studied by Nothern blot analysis. Northern blot analysis of vanadium oxide treated cells showed decreasing effects 0& sodium orthovanadate revealed increasing effects in type I $\alpha$ 2 collagen ribonucleic acid (mRNA) level.

• Journal of Microbiology and Biotechnology
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• v.19 no.9
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• pp.918-921
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• 2009

In the present study, we examined the inhibitory effects of protein tyrosine phosphatase (PTPase) inhibitors, including sodium orthovanadate (SOV), ammonium molybdate (AM), and iodoacetamide (IA), on cell growth, accumulation of astaxanthin, and PTPase activity in the photosynthetic algae Haematococcus lacustris. PTPase activity was assayed spectrophotometrically and was found to be inhibited 60% to 90% after treatment with the inhibitors. SOY markedly abolished PTPase activity, significantly activating the accumulation of astaxanthin. These data suggest that the accumulation of astaxanthin in H. lacustris results from the concerted actions of several PTPases.

• Proceedings of the Zoological Society Korea Conference
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• 1994.10a
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• pp.156.1-156
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• 1994

• BMB Reports
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• v.55 no.8
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• pp.389-394
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• 2022

In particular, the phenomenon of c-Jun degradation within the inflammatory response has not yet been fully analyzed. In order to verify this, we investigated LPS-stimulated murine macrophages pre-treated with sodium orthovanadate (SO) in order to uncover the regulatory mechanisms of the MAPKs which regulate c-Jun degradation within the inflammatory response. Through our study, we found that SO suppressed the production of prostaglandin E₂ (PGE₂) and the expression of COX-2 in LPS-stimulated RAW264.7 cells. Additionally, SO decreased total c-Jun levels, without altering the amount of mRNA, although the phospho-levels of p38, ERK, and JNK were strongly enhanced. Through the usage of selective MAPK inhibitors, and knockdown and overexpression strategies, p38 was revealed to be a major MAPK which regulates c-Jun degradation. Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment. Therefore, our results suggest that the hyperphosphorylation of p38 by SO contributes to c-Jun degradation, which is linked to the suppression of PGE₂ secretion in inflammatory responses; and thus, finding drugs to increase p38 activity could be a novel strategy for the development of anti-inflammatory drugs.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.135.2-135.2
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• 2003

Plasma membrane blebs are observed in many types of apoptotic cells, but their processes of formation remain to be clarified. In the present study, we investigated whether there is a relationship between change of intracellular phosphotyrosine levels and biochemical apoptotic events in Jurkat T cells undergoing apoptosis by agonistic anti-Fas antibody. When Jurkat cells were treated with Fas-antibody in the presence or absence of pretreatment with sodium orthovanadate ($Na_3${VO}_4$), a phosphotyrosine phosphatase (PTPase) inhibitor, membrane blebs disappeared in orthovanadate-treated cells. (omitted)

• Toxicological Research
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• v.7 no.2
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• pp.239-255
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• 1991

Several types of IFNs were tested for their ability to suppress TCDD-inducible P-450 dependent mixed function oxidase (MFO) system in mouse primary hepatocytes. Mouse IFN-gamma (IFN-G) markedly suppressed EROD activity when added at the same time as TCDD (10 nM). The antagonism of EROD activity by IFN-G exhibited both a dose-(10-100 U/ml) and time-depedence. In contrast, mouse IFN-A/B was only moderately suppressive and only at high concentrations (500 U/ml). Rat IFN-G was even more selective than mouse, wherase human IFN-G had no activity.

• BMB Reports
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• v.45 no.5
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• pp.317-322
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• 2012

2-deoxy-D-glucose(2DG)-caused endoplasmic reticulum (ER) stress inhibits protein phosphorylation at tyrosine residues. However, the accurate regulatory mechanisms, which determine the inflammatory response of chondrocytes to ER stress via protein tyrosine phosphorylation, have not been systematically evaluated. Thus, in this study, we examined whether protein phosphorylation at tyrosine residues can modulate the expression and glycosylation of COX-2, which is reduced by 2DG-induced ER stress. We observed that protein tyrosine phosphatase (PTP) inhibitors, sodium orthovanadate (SOV), and phenylarsine oxide (PAO) significantly decreased expression of ER stress inducible proteins, glucose-regulated protein 94 (GRP94), and CCAAT/ enhancer-binding-protein- related gene (GADD153), which was induced by 2DG. In addition, we demonstrated that SOV and PAO noticeably restored the expression and glycosylation of COX-2 after treatment with 2DG. These results suggest that protein phosphorylation of tyrosine residues plays an important role in the regulation of expression and glycosylation during 2DG-induced ER stress in rabbit articular chondrocytes.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.243-249
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• 2006

The effect of genistein, widely used as a specific tyrosine kinase inhibitor, on rat brain Kv1.5 channels which were stably expressed in Chinese hamster ovary cells was investigated using the whole-cell patch-clamp technique. Genistein inhibited Kv1.5 currents at +50 mV in a concentration-dependent manner, with an $IC_{50}$ of $54.7{\pm}8.2\;{\mu}M$ and a Hill coefficient of $1.1{\pm}0.2$. Pretreatment of Kv1.5 with protein tyrosine kinase inhibitors ($10\;{\mu}M$ lavendustin A and $100\;{\mu}M$ AG1296) and a tyrosine phosphatase inhibitor ($500\;{\mu}M$ sodium orthovanadate) did not block the inhibitory effect of genistein. The inhibition of Kv1.5 by genistein showed voltage-independence over the full activation voltage range positive to 0 mV. The activation (at +50 mV) kinetics was significantly delayed by genistein: time constant for an activation of $1.4{\pm}0.2$ msec under control conditions and $10.0{\pm}1.5$ msec in the presence of $60\;{\mu}M$ genistein. Genistein also slowed the deactivation of the tail currents, resulting in a crossover phenomenon: a time constant of $11.4{\pm}1.3$ msec and $40.0{\pm}4.2$ msec under control conditions and in the presence of $60\;{\mu}M$ genistein, respectively. Inhibition was reversed by the application of repetitive depolarizing pulses, especially during the early part of the activating pulse. These results suggest that genistein directly inhibits Kv1.5 channels, independent of phosphotyrosine-signaling pathway.